Structural MRI and Molecular PET Imaging (AV45 and AV1451) in the Diagnosis of Chronic Traumatic Encephalopathy In Vivo: Study of a Retired NFL Player (P4.046)

Objective: Here we show longitudinal neuropsychological and structural MRI data of a football player who has endured several concussions. We aim to reveal patterns aiding in understanding progression of the disease and informing diagnostic criteria. Background:Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder resulting from repetitive mild brain trauma. Currently, the definite diagnosis of CTE is established postmortem, and studies are needed to facilitate detection during life. Methods:Here we describe the clinical case of a 39-year-old retired National Football League player with a history of 22 concussions and cognitive complaints. Evaluation included neurologic and neuropsychological assessment, structural MRI, [18F]florbetapir amyloid positron emission tomography (PET) imaging, and experimental tau PET imaging with [18F]T807. Additional neuropsychological data from 2010 and a structural MRI from 2011 enabled us to perform longitudinal analyses of neuropsychological performance, cortical thickness, and subcortical volumes. Cognitive performance as assessed by neuropsychological testing, declined over the 5-year period from 2010 to 2015, especially in the domains of executive functioning, verbal fluency, and fine motor skills. Results: Overall performance was below average on tests of narrative memory and naming but was average or higher in other memory and language tests. In longitudinal structural analysis, left frontal areas (Broca’s area, medial orbitofrontal cortex), the lateral temporal areas, and the basal ganglia showed greatest volume losses, with apparent sparing of medial temporal lobe structures. PET imaging was negative for amyloid but revealed possible multifocal [18F]T807 retention, consistent with postmortem patterns of tau deposition in CTE at the junction of cortical grey matter and white matter. Conclusions:Although the definitive identification of the neuropathological retention of [18F]T807 requires postmortem correlation, our data suggests that [18F]T807 may inform future diagnostic criteria for CTE in living patients. Disclosure: Dr. Dickstein has nothing to disclose. Dr. Pullman has nothing to disclose. Dr. Fernandez has nothing to disclose. Dr. Short has nothing to disclose. Dr. Kostakoglu has nothing to disclose. Dr. Knesaurek has nothing to disclose. Dr. Jordan has nothing to disclose. Dr. Gordon has nothing to disclose. Dr. Dams-O9Connor has nothing to disclose. Dr. Delman has nothing to disclose. Dr. Tang has nothing to disclose. Dr. DeKosky has received personal compensation for activities with AstraZeneca and Novartis as a consultant. Dr. Stone has nothing to disclose. Dr. Cantu has nothing to disclose. Dr. Hof has nothing to disclose. Dr. Gandy has received personal compensation for activities with Johnson & Johnson, Pfizer, Diagenic, Amicus, and Baxter.