Abstract

Chronic post-concussive syndromes are a major source of morbidity and mortality and can develop into neurodegenerative disorders such as chronic traumatic encephalopathy (CTE). Methods of assessment and prediction of outcome are major areas of research focus, in particular molecular neuroimaging with positron emission tomography (PET) using ligands for neuropathological lesions such as plaques and tangles. CTE is characterized pathologically by the presence of neurofibrillary tau deposits. In living persons, advances in diagnosis have been made through positron emission tomography (PET) using tracers binding to aggregated tau. Here we examined [18F]T807 uptake in athletes with mild traumatic brain injury resulting from multiple concussions. College and professional athletes were included if they reported >1 concussion and cognitive affective or behavioral complaints. LOC > than an hour was exclusionary. Controls without head injury, psychiatric or neurological conditions were matched to age and gender (all males, 24 athletes age 52 ± 9.589; 4 controls, age 48 ± 5.629). Consented participants were evaluated as part of a research study. All subjects underwent PET for tau ([18F]T807/AV-1451) and amyloid ([18F]florbetapir/AV-45), MRI and neuropsychological and clinical assessment. We report here on 24 athletes and 4 controls. There were minimal differences on cognition between athletes and controls and significant differences in behavioral and affective symptoms. All subjects were negative for [18F]florbetapir. Eight of 24 (33%) athletes had abnormal [18F]T807 ligand retention and none of the controls did. While the amount of ligand retention varied in athletes, the pattern resembles postmortem CTE, with tau distribution in the sulci. Our study of in vivo imaging of tau deposition in the brains of retired athletes provides insight into the phenomenology and pathogenesis, of CTE. Tauopathy imaging may provide useful diagnostic or prognostic screening information. This research was supported by a grant from the Alzheimer's Disease Drug Foundation.

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