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Degenerative Brain Disease in Contact-Sport Athletes—Scientists Hit Back

  • 12/9/2016 2:20:00 AM
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Degenerative Brain Disease in Contact-Sport Athletes—Scientists Hit Back

Christina Bennett, M.S.

You have probably seen the headlines touting the latest football player to be diagnosed with the rare degenerative brain disease called chronic traumatic encephalopathy (CTE). CTE was first diagnosed in NFL football player Mike Webster in 2002 and has continued to grab the public’s attention.

Experts believe that repeated hits to the head are the cause of CTE. These brain injury events include both those labeled as concussions and brain injuries less severe. People at risk for CTE are those who play contact sports, such as football, soccer, rugby, wrestling, and boxing. Also, people in the military who participate in combat are at risk too. Typically, these at-risk athletes and military personnel have acquired several brain injuries for many years.

One challenge with learning more about CTE is the condition can be diagnosed only after death because an autopsy is needed to look for specific changes in the brain. Also, no such cure exists, making research that studies this disease particularly warranted. As such, preventing brain injuries in the first place, and in turn lowering the risk for CTE, is key.

Symptoms of CTE often do not show for years, even decades, after repeated head injuries. Some symptoms include difficulty thinking, changes in behavior (such as aggression, depression, and suicidal actions), memory loss, and reduced motor function. As CTE progresses, dementia may occur. Often, people mistake some of these symptoms as signs of aging.

In a person with CTE, the brain is slowly deteriorating and eventually loses tissue mass. In fact, the progression of CTE can be broken down into four stages, and by the fourth stage, the brain mass has decreased by 50 percent. Tau protein, a molecule that forms deposits and distinct tangles in a brain afflicted with CTE, is believed to play a role. Tau protein function is also disrupted in Alzheimer’s disease, but the pattern of tau deposits and tangles in CTE is different from what is seen in Alzheimer’s.

The good news is researchers are making strides. For the first time, authors of a recent study linked brain inflammation in football athletes to CTE. To conduct the study, authors selected 66 former football players who had died and donated their brains to a brain bank and 16 non-athletes to serve as the control group. This study was published in the journal Acta Neuropathologica Communications on October 28, 2016.

Specifically, Jonathan Cherry and the other study authors found that the longer an athlete played the high-contact game, the greater the risk of developing CTE. With each brain injury comes inflammation, which is the body’s way of protecting the brain, but these repeat brain injuries and therefore prolonged inflammation may be the reason why CTE develops. The potential for these findings is that molecules that participate in inflammation could help diagnosis CTE in living people and even be targets for treatments.

However, not all experts accept these findings just yet. More research is needed to determine how exactly CTE develops. Inflammation is not the only process that occurs after brain injury, so other processes could be involved too. Also, this particular study was limited by its being retrospective, meaning the researchers looked at events in the past, and the brain tissue studied was that of athletes who chose to donate, not those who were randomly selected.

Despite these limitations, previous findings support this study’s reasoning. For example, in an earlier study, these authors showed that the number of years of repeated head injuries correlated with a higher stage of CTE in athletes and military personnel. Also, other researchers have shown molecules involved in brain inflammation for degenerative brain diseases to promote tau protein disarray, suggesting brain injury and CTE are linked. Findings have also linked degenerative brain diseases to brain inflammation. Future studies are certainly needed, but this one serves as a good start.

References:

  1. Cherry JD, Tripodis Y, Alvarez VE, et al. Microglial neuroinflammation contributes to tau accumulation in chronic traumatic encephalopathy. Acta Neuropathologica Communications. 2016;4:112.

  2. McKee AC, Stein TD, Kiernan PT, Alvarez VE. The neuropathology of chronic traumatic encephalopathy. Brain Pathol. 2015;25(3):350-364.

  3. McKee AC, Cantu RC, Nowinski CJ, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy following repetitive head injury. J Neuropathol Exp Neurol. 2009;68(7): 709-735.

  4. Safinia C, Bershad EM, Clark HB, et al. Chronic Traumatic Encephalopathy in Athletes Involved with High-impact Sports. J Vasc Interv Neurol. 2016;9(2):34-48.

  5. What is CTE? Concussion Legacy Foundation website. http://concussionfoundation.org/learning-center/what-is-cte. Accessed 11/11/16.

  6. Chronic traumatic encephalopathy. Mayo Clinic website. http://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/basics/definition/con-20113581. Accessed 11/11/16.

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