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[PMID]:28742910
[Au] Autor:Mez J; Daneshvar DH; Kiernan PT; Abdolmohammadi B; Alvarez VE; Huber BR; Alosco ML; Solomon TM; Nowinski CJ; McHale L; Cormier KA; Kubilus CA; Martin BM; Murphy L; Baugh CM; Montenigro PH; Chaisson CE; Tripodis Y; Kowall NW; Weuve J; McClean MD; Cantu RC; Goldstein LE; Katz DI; Stern RA; Stein TD; McKee AC
[Ad] Endereço:Boston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, Massachusetts2Department of Neurology, Boston University School of Medicine, Boston, Massachusetts.
[Ti] Título:Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football.
[So] Source:JAMA;318(4):360-370, 2017 07 25.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Players of American football may be at increased risk of long-term neurological conditions, particularly chronic traumatic encephalopathy (CTE). Objective: To determine the neuropathological and clinical features of deceased football players with CTE. Design, Setting, and Participants: Case series of 202 football players whose brains were donated for research. Neuropathological evaluations and retrospective telephone clinical assessments (including head trauma history) with informants were performed blinded. Online questionnaires ascertained athletic and military history. Exposures: Participation in American football at any level of play. Main Outcomes and Measures: Neuropathological diagnoses of neurodegenerative diseases, including CTE, based on defined diagnostic criteria; CTE neuropathological severity (stages I to IV or dichotomized into mild [stages I and II] and severe [stages III and IV]); informant-reported athletic history and, for players who died in 2014 or later, clinical presentation, including behavior, mood, and cognitive symptoms and dementia. Results: Among 202 deceased former football players (median age at death, 66 years [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87%; median age at death, 67 years [interquartile range, 52-77 years]; mean years of football participation, 15.1 [SD, 5.2]), including 0 of 2 pre-high school, 3 of 14 high school (21%), 48 of 53 college (91%), 9 of 14 semiprofessional (64%), 7 of 8 Canadian Football League (88%), and 110 of 111 National Football League (99%) players. Neuropathological severity of CTE was distributed across the highest level of play, with all 3 former high school players having mild pathology and the majority of former college (27 [56%]), semiprofessional (5 [56%]), and professional (101 [86%]) players having severe pathology. Among 27 participants with mild CTE pathology, 26 (96%) had behavioral or mood symptoms or both, 23 (85%) had cognitive symptoms, and 9 (33%) had signs of dementia. Among 84 participants with severe CTE pathology, 75 (89%) had behavioral or mood symptoms or both, 80 (95%) had cognitive symptoms, and 71 (85%) had signs of dementia. Conclusions and Relevance: In a convenience sample of deceased football players who donated their brains for research, a high proportion had neuropathological evidence of CTE, suggesting that CTE may be related to prior participation in football.
[Mh] Termos MeSH primário: Traumatismos em Atletas/patologia
Encéfalo/patologia
Encefalopatia Traumática Crônica/patologia
Futebol Americano/lesões
[Mh] Termos MeSH secundário: Adulto
Idoso
Atletas
Traumatismos em Atletas/complicações
Concussão Encefálica/epidemiologia
Causas de Morte
Encefalopatia Traumática Crônica/diagnóstico
Encefalopatia Traumática Crônica/etiologia
Transtornos Cognitivos/etiologia
Seres Humanos
Masculino
Transtornos Mentais/etiologia
Meia-Idade
Índice de Gravidade de Doença
Transtornos Relacionados ao Uso de Substâncias/etiologia
Estados Unidos
Proteínas tau/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (tau Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.8334


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[PMID]:29260223
[Au] Autor:McKee AC; Mez J; Abdolmohammadi B
[Ad] Endereço:Boston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, Massachusetts.
[Ti] Título:Chronic Traumatic Encephalopathy in Football Players-Reply.
[So] Source:JAMA;318(23):2353, 2017 12 19.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Encefalopatia Traumática Crônica
Futebol Americano
[Mh] Termos MeSH secundário: Seres Humanos
Futebol
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.16687


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[PMID]:29260221
[Au] Autor:Yari N
[Ad] Endereço:Baylor Scott and White Medical Center, Dallas, Texas.
[Ti] Título:Chronic Traumatic Encephalopathy in Football Players.
[So] Source:JAMA;318(23):2352-2353, 2017 12 19.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Encefalopatia Traumática Crônica
Futebol Americano
[Mh] Termos MeSH secundário: Seres Humanos
Futebol
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.16675


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[PMID]:29260220
[Au] Autor:Zuckerman SL; Brett BL; Yengo-Kahn AM
[Ad] Endereço:Vanderbilt Sports Concussion Center, Vanderbilt University School of Medicine, Nashville, Tennessee.
[Ti] Título:Chronic Traumatic Encephalopathy in Football Players.
[So] Source:JAMA;318(23):2352, 2017 12 19.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Encefalopatia Traumática Crônica
Futebol Americano
[Mh] Termos MeSH secundário: Seres Humanos
Futebol
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.16667


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[PMID]:29016093
[Au] Autor:Ray JW; Hwang C; Baine J; Fredericson M; Keane GP
[Ti] Título:Current Concepts in Concussion: A Review.
[So] Source:J Calif Dent Assoc;45(6):285-89, 2017 06 22.
[Is] ISSN:1043-2256
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Concussão Encefálica/diagnóstico
Concussão Encefálica/terapia
[Mh] Termos MeSH secundário: Traumatismos em Atletas/diagnóstico
Traumatismos em Atletas/terapia
Encefalopatia Traumática Crônica/etiologia
Seres Humanos
Protetores Bucais
Síndrome Pós-Concussão/prevenção & controle
Aposentadoria
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:D
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE


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[PMID]:28975240
[Au] Autor:Asken BM; Sullan MJ; DeKosky ST; Jaffee MS; Bauer RM
[Ad] Endereço:Department of Clinical and Health Psychology, University of Florida, Gainesville.
[Ti] Título:Research Gaps and Controversies in Chronic Traumatic Encephalopathy: A Review.
[So] Source:JAMA Neurol;74(10):1255-1262, 2017 Oct 01.
[Is] ISSN:2168-6157
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Scientific and lay interest in negative outcomes associated with exposure to repetitive brain trauma (RBT) continues to strengthen. Concerns about the association between RBT and dementia began more than a century ago, but have resurfaced in the last decade with the more recently described chronic traumatic encephalopathy (CTE). Chronic traumatic encephalopathy is a tauopathy associated with RBT that has become inextricably linked to conversations about sport-related concussion and mild traumatic brain injury. Accordingly, specific populations such as collision sport athletes and certain military personnel are of particular interest owing to their unique exposure to RBT. The gaps and controversies in our understanding of the epidemiologic factors, mechanism, and clinicopathological correlates of CTE reflect the current reliance on postmortem case series investigations. This review discusses the state of the science of CTE and raises considerations for researching and interpreting cognitive changes in members of at-risk populations. Observations: The recent development of pathological diagnostic criteria for CTE represented an important step for differentiating CTE from other neurodegenerative diseases. By comparison, defining the clinical syndrome(s) associated with CTE and the necessary and sufficient symptoms needed for its diagnosis lags behind. The absence of validated in vivo biomarkers of pathological characteristics of CTE and longitudinal tracking with neuropsychological evaluation remains a significant hurdle. Attribution of candidate symptoms in retired athletes to CTE is complicated by the presence of multiple premorbid and comorbid factors affecting cognitive reserve that influence normal or expected cognitive functioning. This is a critical issue in appropriately defining reference groups for normative comparisons. Conclusions and Relevance: Available data, while limited and complicated by selection bias, indicate that exposure to RBT represents the greatest risk factor for CTE pathological features, although clinicopathological correlates and the nature of onset and progression of symptoms are largely unknown. Considering aspects of cognitive reserve is likely essential for both interpreting cognitive outcomes associated with CTE and for developing preventive treatment programs. Research on CTE would benefit greatly from incorporating principles established within other areas of neurodegenerative disease and the nuances of clinicopathological considerations.
[Mh] Termos MeSH primário: Encefalopatia Traumática Crônica/complicações
Encefalopatia Traumática Crônica/diagnóstico
[Mh] Termos MeSH secundário: Traumatismos em Atletas/complicações
Traumatismos em Atletas/epidemiologia
Pesquisa Biomédica
Encefalopatia Traumática Crônica/epidemiologia
Encefalopatia Traumática Crônica/psicologia
Transtornos Cognitivos/etiologia
Seres Humanos
Saúde Pública/estatística & dados numéricos
Saúde Pública/tendências
Suicídio/psicologia
Suicídio/estatística & dados numéricos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1001/jamaneurol.2017.2396


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[PMID]:28950005
[Au] Autor:Cherry JD; Stein TD; Tripodis Y; Alvarez VE; Huber BR; Au R; Kiernan PT; Daneshvar DH; Mez J; Solomon TM; Alosco ML; McKee AC
[Ad] Endereço:Boston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, United States of America.
[Ti] Título:CCL11 is increased in the CNS in chronic traumatic encephalopathy but not in Alzheimer's disease.
[So] Source:PLoS One;12(9):e0185541, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CCL11, a protein previously associated with age-associated cognitive decline, is observed to be increased in the brain and cerebrospinal fluid (CSF) in chronic traumatic encephalopathy (CTE) compared to Alzheimer's disease (AD). Using a cohort of 23 deceased American football players with neuropathologically verified CTE, 50 subjects with neuropathologically diagnosed AD, and 18 non-athlete controls, CCL11 was measured with ELISA in the dorsolateral frontal cortex (DLFC) and CSF. CCL11 levels were significantly increased in the DLFC in subjects with CTE (fold change = 1.234, p < 0.050) compared to non-athlete controls and AD subjects with out a history of head trauma. This increase was also seen to correlate with years of exposure to American football (ß = 0.426, p = 0.048) independent of age (ß = -0.046, p = 0.824). Preliminary analyses of a subset of subjects with available post-mortem CSF showed a trend for increased CCL11 among individuals with CTE (p = 0.069) mirroring the increase in the DLFC. Furthermore, an association between CSF CCL11 levels and the number of years exposed to football (ß = 0.685, p = 0.040) was observed independent of age (ß = -0.103, p = 0.716). Finally, a receiver operating characteristic (ROC) curve analysis demonstrated CSF CCL11 accurately distinguished CTE subjects from non-athlete controls and AD subjects (AUC = 0.839, 95% CI 0.62-1.058, p = 0.028). Overall, the current findings provide preliminary evidence that CCL11 may be a novel target for future CTE biomarker studies.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Biomarcadores/metabolismo
Encéfalo/metabolismo
Quimiocina CCL11/metabolismo
Encefalopatia Traumática Crônica/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Futebol Americano/lesões
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CCL11 protein, human); 0 (Chemokine CCL11)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185541


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[PMID]:28920887
[Au] Autor:Wilson L; Stewart W; Dams-O'Connor K; Diaz-Arrastia R; Horton L; Menon DK; Polinder S
[Ad] Endereço:Division of Psychology, University of Stirling, Stirling, UK. Electronic address: j.t.l.wilson@stir.ac.uk.
[Ti] Título:The chronic and evolving neurological consequences of traumatic brain injury.
[So] Source:Lancet Neurol;16(10):813-825, 2017 Oct.
[Is] ISSN:1474-4465
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Traumatic brain injury (TBI) can have lifelong and dynamic effects on health and wellbeing. Research on the long-term consequences emphasises that, for many patients, TBI should be conceptualised as a chronic health condition. Evidence suggests that functional outcomes after TBI can show improvement or deterioration up to two decades after injury, and rates of all-cause mortality remain elevated for many years. Furthermore, TBI represents a risk factor for a variety of neurological illnesses, including epilepsy, stroke, and neurodegenerative disease. With respect to neurodegeneration after TBI, post-mortem studies on the long-term neuropathology after injury have identified complex persisting and evolving abnormalities best described as polypathology, which includes chronic traumatic encephalopathy. Despite growing awareness of the lifelong consequences of TBI, substantial gaps in research exist. Improvements are therefore needed in understanding chronic pathologies and their implications for survivors of TBI, which could inform long-term health management in this sizeable patient population.
[Mh] Termos MeSH primário: Lesões Encefálicas Traumáticas/complicações
Epilepsia Pós-Traumática/etiologia
Transtornos Mentais/etiologia
Doenças Neurodegenerativas/etiologia
Acidente Vascular Cerebral/etiologia
[Mh] Termos MeSH secundário: Encefalopatia Traumática Crônica/etiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


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[PMID]:28641105
[Au] Autor:Giza CC; Prins ML; Hovda DA
[Ad] Endereço:UCLA Brain Injury Research Center, UCLA Steve Tisch BrainSPORT Program, Department of Neurosurgery, David Geffen School of Medicine, Los Angeles, CA 90095, USA; Division of Pediatric Neurology, Department of Pediatrics, UCLA Mattel Children's Hospital, Los Angeles, CA 90095, USA; Interdepartmental Program for Neuroscience, UCLA, Los Angeles, CA 90095, USA; Interdepartmental Program for Biomedical Engineering, UCLA, Los Angeles, CA 90095, USA. Electronic address: cgiza@mednet.ucla.edu.
[Ti] Título:It's Not All Fun and Games: Sports, Concussions, and Neuroscience.
[So] Source:Neuron;94(6):1051-1055, 2017 Jun 21.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Few items grab the public's attention like sports, from extremes of great victory to injury and defeat. No injury currently arouses stronger interest than concussion. Giza et al., discuss how neuroscience can provide balance between physical activity and TBI, and guide thoughtful discourse and policy.
[Mh] Termos MeSH primário: Traumatismos em Atletas/fisiopatologia
Concussão Encefálica/fisiopatologia
Lesões Encefálicas/fisiopatologia
Lesão Encefálica Crônica/fisiopatologia
[Mh] Termos MeSH secundário: Traumatismos em Atletas/metabolismo
Concussão Encefálica/metabolismo
Lesões Encefálicas/metabolismo
Lesões Encefálicas Traumáticas/metabolismo
Lesões Encefálicas Traumáticas/fisiopatologia
Lesão Encefálica Crônica/metabolismo
Encefalopatia Traumática Crônica/metabolismo
Encefalopatia Traumática Crônica/fisiopatologia
Seres Humanos
Neurociências
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE


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[PMID]:28520686
[Au] Autor:Thomsen GM; Ko A; Harada MY; Ma A; Wyss L; Haro P; Vit JP; Avalos P; Dhillon NK; Cho N; Shelest O; Ley EJ
[Ad] Endereço:From the Regenerative Medicine Institute (G.M.T., A.M., L.W., P.H., N.C., O.S.), Department of Biomedical Sciences (G.M.T., J-P.V.), and Biobehavioral Research Core (J-P.V.), and Division of Trauma and Critical Care, Department of Surgery (A.K., M.Y.H., N.D., E.J.L.), Cedars-Sinai Medical Center, Los Angeles, California.
[Ti] Título:Clinical correlates to assist with chronic traumatic encephalopathy diagnosis: Insights from a novel rodent repeat concussion model.
[So] Source:J Trauma Acute Care Surg;82(6):1039-1048, 2017 Jun.
[Is] ISSN:2163-0763
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repetitive head injuries. Chronic traumatic encephalopathy symptoms include changes in mood, behavior, cognition, and motor function; however, CTE is currently diagnosed only postmortem. Using a rat model of recurrent traumatic brain injury (TBI), we demonstrate rodent deficits that predict the severity of CTE-like brain pathology. METHODS: Bilateral, closed-skull, mild TBI was administered once per week to 35 wild-type rats; eight rats received two injuries (2×TBI), 27 rats received five injuries (5×TBI), and 13 rats were sham controls. To determine clinical correlates for CTE diagnosis, TBI rats were separated based on the severity of rotarod deficits and classified as "mild" or "severe" and further separated into "acute," "short," and "long" based on age at euthanasia (90, 144, and 235 days, respectively). Brain atrophy, phosphorylated tau, and inflammation were assessed. RESULTS: All eight 2×TBI cases had mild rotarod deficiency, 11 5×TBI cases had mild deficiency, and 16 cases had severe deficiency. In one cohort of rats, tested at approximately 235 days of age, balance, rearing, and grip strength were significantly worse in the severe group relative to both sham and mild groups. At the acute time period, cortical thinning, phosphorylated tau, and inflammation were not observed in either TBI group, whereas corpus callosum thinning was observed in both TBI groups. At later time points, atrophy, tau pathology, and inflammation were increased in mild and severe TBI groups in the cortex and corpus callosum, relative to sham controls. These injury effects were exacerbated over time in the severe TBI group in the corpus callosum. CONCLUSIONS: Our model of repeat mild TBI suggests that permanent deficits in specific motor function tests correlate with CTE-like brain pathology. Assessing balance and motor coordination over time may predict CTE diagnosis.
[Mh] Termos MeSH primário: Concussão Encefálica/complicações
Encefalopatia Traumática Crônica/diagnóstico
[Mh] Termos MeSH secundário: Animais
Atrofia
Encéfalo/patologia
Concussão Encefálica/patologia
Encefalopatia Traumática Crônica/patologia
Encefalopatia Traumática Crônica/fisiopatologia
Corpo Caloso/patologia
Modelos Animais de Doenças
Masculino
Destreza Motora
Fosforilação
Equilíbrio Postural
Ratos
Ratos Sprague-Dawley
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (tau Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1097/TA.0000000000001443



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