[P4–232]: TAU IMAGING WITH [18F]T807/AV‐1451 IN ATHLETES WITH POST‐CONCUSSIVE COMPLAINT AND CONTROLS

• DOI: 10.1016/j.jalz.2017.06.2100
• Publication Date: 2017-10-20T08:48:18Z
• Authors: Samuel Gandy; Dara Dickstein; Mariel Pullman; Jennifer Short; Lale Kostakoglu; Karin Knesaurek; Barry Jordan; Wayne Gordon; Kristen Dams‐O'Co...; Cheuk Tang; Edmund Wong; Steven DeKosky; James Stone; George Farmer; Elaine R. Peskind; Mary Sano; Patrick R. Hof
• Keywords: Chronic traumatic encephalopathy

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