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Transl Psychiatry. 2016 Sep 27;6(9):e900. doi: 10.1038/tp.2016.175.

Cerebral [18 F]T807/AV1451 retention pattern in clinically probable CTE resembles pathognomonic distribution of CTE tauopathy.

Author information

1
Fishberg Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
2
Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
3
Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
4
Department of Nuclear Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
5
Burke Rehabilitaiton Hospital, White Plains, NY, USA.
6
The NFL Neurological Program, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
7
Department of Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
8
Department of Radiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
9
Department of Neurology, University of Florida, Gainesville, FL, USA.
10
Department of Radiology and Medical Imaging, University of Virginia, Charlottesville, VA, USA.
11
Department of Neurosurgery, University of Virginia, Charlottesville, VA, USA.
12
Centre for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, MA, USA.
13
Department of Neurosurgery, Emerson Hospital, Concord, MA, USA.
14
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Abstract

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder most commonly associated with repetitive traumatic brain injury (TBI) and characterized by the presence of neurofibrillary tangles of tau protein, known as a tauopathy. Currently, the diagnosis of CTE can only be definitively established postmortem. However, a new positron emission tomography (PET) ligand, [18F]T807/AV1451, may provide the antemortem detection of tau aggregates, and thus various tauopathies, including CTE. Our goal was to examine [18F]T807/AV1451 retention in athletes with neuropsychiatric symptoms associated with a history of multiple concussions. Here we report a 39-year-old retired National Football League player who suffered 22 concussions and manifested progressive neuropsychiatric symptoms. Emotional lability and irritability were the chief complaints. Serial neuropsychological exams revealed a decline in executive functioning, processing speed and fine motor skills. Naming was below average but other cognitive functions were preserved. Structural analysis of longitudinally acquired magenetic resonance imaging scans revealed cortical thinning in the left frontal and lateral temporal areas, as well as volume loss in the basal ganglia. PET with [18F]florbetapir was negative for amyloidosis. The [18F]T807/AV1451 PET showed multifocal areas of retention at the cortical gray matter-white matter junction, a distribution considered pathognomonic for CTE. [18F]T807/AV1451 standard uptake value (SUV) analysis showed increased uptake (SUVr⩾1.1) in bilateral cingulate, occipital, and orbitofrontal cortices, and several temporal areas. Although definitive identification of the neuropathological underpinnings basis for [18F]T807/AV1451 retention requires postmortem correlation, our data suggest that [18F]T807/AV1451 tauopathy imaging may be a promising tool to detect and diagnose CTE-related tauopathy in living subjects.

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