Living former NFL players with at least one concussion
or traumatic brain injury had higher levels of the protein marker tau, commonly associated with an increased risk for Alzheimer’s disease, in the parts of the brain that are impacted by chronic traumatic encephalopathy vs. persons who did not experience a head injury, according to findings recently published in The New England Journal of Medicine.
The Concussion Legacy Foundation has previously said that in patients with CTE, tau operates differently, causing brain dysfunction that can lead to mental and neurological conditions.
“Although persons with the neuropathologic features of CTE have been reported to have cognitive impairment, mood disturbance, and behavioral dyscontrol, it is unclear whether these features are associated with ... consequences of brain trauma,” Robert A. Stern, PhD, of the Boston University School of Medicine and colleagues wrote.
Stern and colleagues used tau-ligand positron emission tomography to measure tau and amyloid-beta depositions of 26 former NFL players who had at least one TBI or concussion and these dyscontrols. Their levels were compared to 31 men without such symptoms.
Stern and colleagues found the former NFL players had higher tau levels in the bilateral medial temporal (1.23 vs. 1.12; mean difference, 0.13 [95% CI, 0.05-0.21]), left parietal (1.12 vs. 1.01; mean difference, 0.12 [95% CI, 0.05-0.2]) and bilateral superior frontal (1.09 vs. 0.98; mean difference, 0.13 [95% CI, 0.06-0.2]) sections of the brain vs. the control cohort. No links between neuropsychiatric and cognitive test scores and tau were determined.
“Findings suggest that the cognitive difficulties reported by the former players were not related to Alzheimer’s disease amyloid-beta deposition,” Stern and colleagues wrote.
Living, former NFL players with at least one concussion or traumatic brain injury had higher tau levels in the parts of the brain that are impacted by chronic traumatic encephalopathy vs. persons without such injury, according to findings recently published in The New England Journal of Medicine
“Future studies are needed to determine whether elevated CTE-associated tau can be detected in individual persons,” they added.
In a related editorial, Allen H. Ropper, MD, deputy editor of NEJM wrote that a way to diagnose CTE in living patients is still elusive.
“The CTE field is in a phase of fumbling with circumstantial evidence for a connection between tau deposition and a clinical syndrome. The authors of the current study emphasize that their findings are derived from computational models involving a group of former NFL players compared with a group of controls, and these techniques cannot yet be used to diagnose CTE in an individual player,” he wrote.
“The report ... certainly does strengthen the case that tau is the offender in early CTE, but other techniques remain to be clarified. The techniques for studying living biology, such as this use of tau-ligand [positron emission tomography], are making a difference,” he concluded. – by Janel Miller
Concussion Legacy Foundation. “CTE resources.” https://concussionfoundation.org/CTE-resources. Accessed April 9, 2019.
Concussion Legacy Foundation. “The science of CTE.” https://concussionfoundation.org/CTE-resources/science-of-CTE. Accessed April 9, 2019.
Ropper AH. NEJM. 2019;published online ahead of print.
Stern RA, et al. NEJM. 2019;doi:10.1046/NEJMoa1900757.
Disclosures: Stern reports grant support from Avid Radiopharmaceuticals and NIH. Please see the study for all other authors’ relevant financial disclosures.