PET brain scans of living former NFL players with cognitive and neuropsychiatric symptoms showed higher tau levels than controls in brain regions typically affected by chronic traumatic encephalopathy (CTE), according to an April 11 study published in the New England Journal of Medicine (NEJM).
Flortaucipir PET revealed higher amounts of tau in three areas of the brain—bilateral superior frontal, bilateral medial temporal and left parietal—of 26 former NFL players compared to 31 healthy controls with no history of traumatic brain injury.
“The group of living former NFL players with cognitive, mood, and behavioral symptoms who were examined in this study had elevated flortaucipir PET measurements in regions of the brain that were consistent with the distribution of tau in persons with CTE confirmed by postmortem examination,” wrote first author Robert A. Stern PhD, Boston University School of Medicine, and colleagues.
Typically such tau PET changes associated with CTE have only been measurable during postmortem exams. The new findings could change how clinicians approach the disease.
“Detection of the disease during life could be used to assess its epidemiology, risk factors, and course and could be used in treatment and prevention trials,” the authors added.
In addition to finding higher tau levels in three brain regions, the authors performed an exploratory analysis and found correlation coefficients between 0.45 and 0.58 for the number of years playing tackle football and level of tau deposition.
Tackle football has been proven to dramatically affect the brain development of younger players, and neuropathological studies involving former football players has found the number of years of tackle football played to be associated with the severity of tau deposition, wrote the researchers in the introduction to their study.
Additionally, the NFL players did not have a higher proportion of positive florbetapir PET scans or higher amyloid-beta deposition compared to controls.
“These findings suggest that the cognitive difficulties reported by the former players were not related to Alzheimer’s disease amyloid-beta deposition,” the authors wrote.
Like Alzheimer’s disease, the science on CTE “is in a phase of fumbling with circumstantial evidence for a connection between tau deposition and a clinical syndrome,” wrote Allan H. Ropper, MD, deputy editor of NEJM, in an accompanying editorial.
“The report in this issue certainly does strengthen the case that tau is the offender early in CTE, but other links remain to be clarified. The techniques for studying living biology, such as this use of tau-ligand PET, are making a difference,” he added.
The study was partially funded by grants from Avid Radiopharmaceuticals.