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.
Highlights
Traumatic brain injury (TBI) is associated with an increased risk of developing dementia, including Alzheimer’s disease (AD).[1,2] recent research in postmortem samples suggests that a separate neurodegenerative syndrome, chronic traumatic encephalopathy (CTE), might be the cause of decline in some individuals who have sustained both single and multiple concussive and subconcussive blows to the head.[3,4] Chronic traumatic encephalopathy (CTE), which was first observed in ‘punch drunk’ boxers[5] and termed ‘dementia pugilistica’,6 is a neurodegenerative disease seen in individuals with a history of repetitive brain trauma, that is, blows to the head.CTE is characterized neuropathologically by progressive deposition of neurofibrillary tangles of hyperphosphorylated tau.[4]
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
The [18F]T807/AV1451 positron emission tomography (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
Summary
Traumatic brain injury (TBI) is associated with an increased risk of developing dementia, including Alzheimer’s disease (AD).[1,2] recent research in postmortem samples suggests that a separate neurodegenerative syndrome, chronic traumatic encephalopathy (CTE), might be the cause of decline in some individuals who have sustained both single and multiple concussive and subconcussive blows to the head.[3,4] CTE, which was first observed in ‘punch drunk’ boxers[5] and termed ‘dementia pugilistica’,6 is a neurodegenerative disease seen in individuals with a history of repetitive brain trauma, that is, blows to the head. Individuals with CTE can display symptoms that overlap with those seen in AD, such as impairments in memory and executive function, but, in contrast to AD, CTE is more frequently characterized by irritability, emotional lability, aggression, impulsivity, suicidality and substance abuse.[7,10,11] Changes in mood and behavior typically precede cognitive decline in CTE, clinical presentation is highly variable.7,11Although individuals with CTE are at risk for severe functional impairment as well as disabling and life-threatening behavioral disturbances; currently, the disease can only be definitively diagnosed at postmortem.[11] Because of this limitation, the discovery of reliable and valid body fluid and/or neuroimaging biomarkers is crucial to.
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