Update – August 18, 2015 – another useful discussion was recently published in the text “Brain Neurotrauma” confirming that more insight into CTE is needed with the authors noting “Despite extensive publicity, the real risk of CTE among amateur and professional players has not been measured or adequately characterized and notions derived from autopsy studies, although useful for understanding mechanisms, cannot give an accurate picture of the range of outcomes after repeat concussions and are limited because of ascertainment bias”
As recently discussed, science does not have a clear understanding of how many hits are too many when it comes to a career in combative sports. What is known, however, is that an accumulation of trauma, both concussive and sub-concussive, play a role in the development of CTE.
A study was recently published in the Journal of Current Pain and Headache Reports titled “Concussion in Chronic Traumatic Encephalopathy” confirming this understanding.
The authors note that “Overall, the number of years of exposure, not the number of concussions, was significantly associated with worse tau pathology in CTE. This suggests that it is the chronic and repetitive nature of head trauma, irrespective of concussive symptoms, that is the most important driver of disease.”
The study’s Abstract, which can be found here (I can’t republish the full study yet as it is behind a paywall) notes:
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive mild traumatic brain injury. It is associated with a variety of clinical symptoms in multiple domains, and there is a distinct pattern of pathological changes. The abnormal tau pathology in CTE occurs uniquely in those regions of the brain that are likely most susceptible to stress concentration during trauma. CTE has been associated with a variety of types of repetitive head trauma, most frequently contact sports. In cases published to date, the mean length of exposure to repetitive head trauma was 15.4 years. The clinical symptoms of the disease began after a mean latency of 14.5 years with a mean age of death of 59.3 years. Most subjects had a reported history of concussions with a mean of 20.3. However, 16 % of published CTE subjects did not have a history of concussion suggesting that subconcussive hits are sufficient to lead to the development of CTE. Overall, the number of years of exposure, not the number of concussions, was significantly associated with worse tau pathology in CTE. This suggests that it is the chronic and repetitive nature of head trauma, irrespective of concussive symptoms, that is the most important driver of disease. CTE and exposure to repetitive head trauma is also associated with a variety of other neurodegenerations, including Alzheimer disease. In fact, amyloid β peptide deposition is altered and accelerated in CTE and is associated with worse disease. Here, we review the current exposure, clinical, and pathological associations of CTE.