A recent UCLA study, appearing in the April 6 online edition of the Proceedings of the National Academy of Science, has taken a step towards earlier detection of Chronic Traumatic Encephalopathy.
Although there is no definitive diagnosis test for CTE in living individuals, this new work has shown how a Tau-sensitive brain imaging agent (F-18)FDDNP, may be able to detect the disease in living people with varying degrees of symptoms. It is felt that early detection could then facilitate effective management strategies and also provide a baseline to measure the effectiveness of such treatments.
Currently, CTE can only be diagnosed definitively following autopsy by finding abnormal proteins, primarily tau, in regions of the brain that control mood, cognition, and motor function. Tau is also one of the abnormal proteins found in the brains of Alzheimer’s patients.
The researches found that the distribution pattern of the abnormal brain proteins (primarily tau) observed in PET scans was distinctly different between concussed patients, Alzheimer’s patients, and normal controls and further posited that such patterns could represent a “fingerprint characteristic of CTE.”
The study involving 14 retired NFL players who had sustained at least one concussion, comparing them to 28 normal people and 24 patients with known Alzheimer’s disease further revealed:
- The PET scans of retired football players showed tau deposits patterns consistent with those observed in autopsy studies of people with CTE.
- Compared with healthy people and those with Alzheimer’s, the football players had higher levels of tau-associated abnormalities in the areas of the brain that control memory, behavior, emotions, and other mental and physical functions.
- Athletes who experienced more concussions had higher amounts of abnormal tau-related imaging.
Additional studies are planned to include multi-site studies to follow subjects over time and determine how effectively this imaging can predict future symptoms.
Although this study focused on retired NFL players, it is interesting to further speculate about:
- How do these findings relate to individuals sustaining concussions in non-athletic pursuits?
- Would a concussion earlier in life make one more susceptible to such abnormal changes if a concussion were sustained later, even much later?
- If enough rest was allowed, or appropriate treatment provided; would this affect the degree of abnormal protein accumulation?
The above questions are just the tip of the iceberg and, hopefully, over time we will find more answers as our understanding of the effects of concussions advances.
- Error: C Jorge R. Barrio, Gary W. Small, Koon-Pong Wong, Sung-Cheng Huang, Jie Liu, David A. Merrill, Christopher C. Giza, Robert P. Fitzsimmons, Bennet Omalu, Julian Bailes, and Vladimir Kepe. In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging. PNAS, April 2015 DOI: 10.1073/pnas.1409952112