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dc.contributor.authorMcKee, Ann C.
dc.contributor.authorCantu, Robert C.
dc.contributor.authorNowinski, Christopher J.
dc.contributor.authorHedley-Whyte, E. Tessa
dc.contributor.authorGavett, Brandon E.
dc.contributor.authorBudson, Andrew E.
dc.contributor.authorSantini, Veronica E.
dc.contributor.authorLee, Hyo-Soon
dc.contributor.authorKubilus, Caroline A.
dc.contributor.authorStern, Robert A.
dc.date.accessioned2017-05-17T16:55:01Z
dc.date.issued2009
dc.identifierQuick submit: 2017-03-22T11:20:49-0400
dc.identifier.citationMcKee, Ann C., Robert C. Cantu, Christopher J. Nowinski, E. Tessa Hedley-Whyte, Brandon E. Gavett, Andrew E. Budson, Veronica E. Santini, Hyo-Soon Lee, Caroline A. Kubilus, and Robert A. Stern. 2009. “Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy After Repetitive Head Injury.” Journal of Neuropathology & Experimental Neurology 68 (7) (July): 709–735. doi:10.1097/nen.0b013e3181a9d503.en_US
dc.identifier.issn0022-3069en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:32697826
dc.description.abstractSince the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed “dementia pugilistica” and more recently, chronic traumatic encephalopathy (CTE). We review the 47 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 professional athletes: one football player and 2 boxers. Clinically, CTE is associated with memory disturbances, behavioral and personality changes, Parkinsonism, and speech and gait abnormalities. Neuropathologically, CTE is characterized by atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem, with ventricular dilatation and a fenestrated cavum septum pellucidum. Microscopically, there are extensive tau-immunoreactive neurofibrillary tangles, astrocytic tangles, and spindle-shaped and threadlike neurites throughout the brain. The neurofibrillary degeneration of CTE is distinguished from other tauopathies by preferential involvement of the superficial cortical layers, irregular, patchy distribution in the frontal and temporal cortices, propensity for sulcal depths, prominent perivascular, periventricular and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes. Deposition of beta amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases. CTE is a neuropathologically distinct, slowly progressive tauopathy with a clear environmental etiology.en_US
dc.language.isoen_USen_US
dc.publisherOxford University Press (OUP)en_US
dc.relation.isversionof10.1097/nen.0b013e3181a9d503en_US
dc.relation.hasversionhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2945234/en_US
dash.licenseLAA
dc.subjectAthletesen_US
dc.subjectConcussionen_US
dc.subjectDementiaen_US
dc.subjectEncephalopathyen_US
dc.subjectNeurodegenerationen_US
dc.subjectTau proteinen_US
dc.subjectTraumatic brain injuryen_US
dc.titleChronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy After Repetitive Head Injuryen_US
dc.typeJournal Articleen_US
dc.date.updated2017-03-22T15:20:54Z
dc.description.versionAccepted Manuscripten_US
dc.relation.journalJournal of Neuropathology & Experimental Neurologyen_US
dash.depositing.authorHedley-Whyte, E. Tessa
dc.date.available2009
dc.date.available2017-05-17T16:55:01Z
dc.identifier.doi10.1097/nen.0b013e3181a9d503*
dash.contributor.affiliatedHedley-Whyte, E.
dash.contributor.affiliatedBudson, Andrew


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