A brain-imaging technique may enable the early detection of chronic traumatic encephalopathy (CTE), according to a study published April 6 in the Proceedings of the National Academy of Sciences.
CTE is a neurodegenerative disease characterized by cognitive and behavioral symptoms linked to traumatic brain injury. One major hallmark of CTE is the abnormal accumulation of tau protein aggregates in brain areas tied to mood and cognition; however, there is currently no definitive approach for clinically diagnosing the condition in living humans.
Bennet Omalu, one of the authors of the study, is chief medical examiner of San Joaquin County and a clinical professor of pathology and laboratory medicine at UC Davis Medical Center. Omalu discovered CTE more than 10 years ago while conducting an autopsy on a retired professional football player that revealed neuropathological changes consistent with long-term repetitive concussive brain injury. He since has found the condition in other football players, wrestlers and veterans, igniting controversy and national interest in the appropriate safety measures.
In the current study, a team of researchers led by UCLA used a brain-imaging technique called positron emission tomography (PET) to detect abnormal protein aggregates in 14 retired professional American football players with an increased risk of developing CTE due to repetitive concussions and sub-concussions, as well as persistent cognitive and behavioral problems.
By injecting a tau-sensitive brain-imaging agent into the participants during PET scanning, the authors detected greater tau accumulation in the dorsal midbrain and the amygdala (regions involved in regulating pain and negative emotions) in the football players, compared with control participants with normal cognitive abilities and patients with Alzheimer’s disease, which may be misdiagnosed as CTE.
The researchers say that the findings could help lead to better identification of brain disorders in athletes and would allow doctors and scientists to test treatments that might help delay the progression of the disease before significant brain damage and symptoms emerge.
Other authors of the paper, "In vivo characterization of Chronic Traumatic Encephalopathy (CTE) using [F-18]FDDNP-PET brain imaging," include Gary W. Small, Koon-Pong Wong, Sung-Cheng Huang, Jie Liu, Christopher C.Giza and David A. Merrill of UCLA; Robert P Fitzsimmons of Fitzsimmons Law Offices in Wheeling, West Virginia; Julian Bailes of NorthShore University Health System; and Vladimir Kepe of the University of Chicago Pritzker School of Medicine.
This study was supported by grants from the NIH (P01-AG025831 and M01-RR00865) and gifts to UCLA from the Toulmin Foundation and Robert and Marion Wilson. No company provided research funding for this study.
The FDDNP marker used with brain PET scans to identify abnormal proteins is intellectual property owned by UCLA and licensed to TauMark, LLC. UCLA authors Barrio, Small and Huang are co-inventors of the PET marker. Barrio, Small, Fitzsimmons and Omalu have a financial interest in the company. Other disclosures are available in the manuscript.