Recent Advances in Understanding CTE in Football Players

Chronic traumatic encephalopathy (CTE) is a degenerative and devastating brain disease that mostly affects military veterans, athletes, and other people who have had cerebral trauma repeatedly. According to Tharmaratnam et al. (2018), CTE was initially demonstrated in 1928 by Martland, who showed how repeated blows on the head result in punch-drunk syndrome using boxers. The effects of this condition can last over a long time, even in the absence of head trauma. Besides, it worsens with age. The diagnosis of this condition can only be done after death by examining tissues of the brain. CTE is prominent among football players. According to research done on 111 diseased NFL players, 110 had it. Understanding CTE among football players involves knowledge of the cause, risk factors, and prevalence of long-term neurological problems. This paper seeks to analyze the available academic material on recent advances in understanding CTE in Football players.

Football players can develop CTE after participating in high school football. However, higher CTE rates have been recorded in pro or college players. According to the Centers for Disease Control and Prevention, over 200, 000 kids between 5 and 18 years old are treated for head injuries related to sports yearly. Beal (2017) note that every year a child plays football increases their risk of contracting CTE. Some of the symptoms of CTE include cognitive changes, dementia, and mood symptoms. It is estimated that 3 million youths play football in the United States today. However, in the past three years, about 47 children have died due to concussive and sub-concussive injuries. Similar research reported that out of 66 brans, 21 showed evidence of CTE in men who played contact football at a young age. 

Most emerging research focuses on concussive injuries resulting from contact sports (Beal, 2017). A highly controlled study was conducted on 25 football players of between 8 and 13 years to explain the consequence of high impact on growing and quickly developing brains (Beal, 2017). In the research, every child was given a helmet (Head Impact Telemetry System) that was fitted with sensors that detect the severity and frequency of head impacts. Practices and games were recorded to measure the severity and the frequency of impacts. Subsequently, the post and pre-season MRI scans were taken and compared. Beal (2017) reveals that there was a significant relationship between changes in brain white matter and head impact exposure. However, there was no definitive diagnosis of concussions.

Senecal, Gurchiek, and Slattery (2017) provide a fifty-year literature review of the research done on the psychological struggles of football players. Many scientists who study CTE have acknowledged that the symptoms of this condition cannot be seen until between 6 and 15 years after the victims have left the field of play and the career. Alongside CTE research, Senecal, Gurchiek, and Slattery (2017) research on psychological struggles that players undergo after transitioning and retiring from the career. The research revealed that there are a variety of symptoms that are similar to those exhibited by CTE patients.

Former contact sports athletes have exhibited psychological symptoms such as lack of motivation, bipolar, irritability, rage, depression, memory loss, mania, and became emotionally unstable. Also, according to Beal (2017), sportsmen who have had no or minimal head impact during their playing days had these very symptoms. Baugh et al. (2014) point out that to-date evidence shows that symptoms of CTE are clinically presented in four possible domains: behavior, motor, cognition, and mood. Players who experienced head trauma and are having symptoms associated with CTE are faced with two tremendous challenges in their lives. The first challenge, as Senecal, Gurchiek, and Slattery (2017) highlight, is living with no CTE diagnosis. Therefore, these individuals are left wondering whether they have the condition or not. All CTE cases are diagnosed postmortem. Although there are hopes for a living diagnosis in the future, many former athletes are experiencing symptoms associated with the condition, and there is no precise diagnosis. Senecal, Gurchiek, and Slattery (2017) acknowledges that there is also a tremendous unsolved problem associated with people with CTE. Until now, there are no discussions for probable biological interventions that can reduce or alleviate the symptoms or occurrence of CTE. The warranted optimism for a living diagnosis does not provide hope for possible biological intervention. 

Tharmaratnam et al. (2018) believe that apart from repetitive brain trauma, generic susceptibility also predisposes an athlete to the development of CTE. A 34-kDa glycosylated protein known as Apolipoprotein ( Apoε) plays an essential role of cholesterol movement in neuronal repair in the brain. Research on the Apoε allele reveals that people who have protein have increased poor functional outcome risk. Tharmaratnam et al. (2018) record that Apoε4 variant is related to greater cognitive deficits, longer healing from brain trauma, and increased severity of the injury. The author also suggests that Apoε4 individuals who play football have not as good clinical outcomes in comparison to other forms of the allele. Over 50% of reported CTE cases are found in people who have the Apoε4 allele. Besides, the allele is associated with depositions of β-amyloid in CTE. However, Tharmaratnam et al. (2018) also note that the variation of Apoε in people with CTE is not extremely huge as compared to that of the people without this condition.

Beal (2017) suggests that although higher CTE cases are recorded in college and pro players, most young people who play football die at a young age due to CTE. Research done on most ex-NFL players confirmed a positive relationship between the age at which players are exposed to contact football and psychiatric and neurological dysfunction as they grow old ( Tharmaratnam et al., 2018) . Children and adolescents experience immense neurological maturation and development. Tharmaratnam et al. (2018) believe that the ages between 9 and 12 years are associated with peak volumes of white and gray matter in the brain. At this time, there is the maturation of the amygdala and hippocampus. The brain becomes vulnerable at this critical time, and it might be exploited by tackle football. Tharmaratnam et al. (2018) also note that some researchers argue that the behavioral dysfunction of the brain due to frequent impact can be compensated through neuroplasticity.

Most to-date scientific literature on cases of CTE shows that the condition is derived from the disease's case series (Baugh et al., 2014). The good news is that the neuropathology of this condition is continually well defined. A research done by McKee in 2013 is listed as the largest case report on people with CTE that is neuropathologically confirmed (Baugh et al., 2014). Baugh et al. (2014) propose a criterion for four CTE pathology stages, based on how severe the findings were. Reliability and formal validation of the staging system used, and these criteria are still underway. The authors have also stated that early CTE cases were more prevalent in motor features that recent reports (Baugh et al., 2014). 

Maroon et al. (2015) has also stated that the knowledge of CTE is considerable progressing with time. However, Baugh et al. (2014) still believe that there are important gaps in CTE research, which include prevalence and incidence of the disease, in vivo diagnostic techniques, and risk factors that are not related to head trauma. According to Maroon et al. (2015), research on CTE is limited to selective case studies. He states that there is no research material that incorporate sport-related and non-sport brain trauma cases. Limited data makes it difficult to monitor and document the occurrence of new cases in contact football. Besides, the general occurrence of this condition among all brain trauma conditions cannot be established by now (Maroon et al., 2015). The fragmented data that has been published cannot assist scientists in concluding the potential risk factors of CTE development in contact football. Maroon et al. (2015) state that all CTE cases that are pathologically confirmed have a head trauma history. However, the documented frequency of impacts, prior concussions, and the degree of severity is highly variable.

Another research that has been done by Ban et al. (2016) reveals that there is no causal relationship between tau protein in the brain and the diagnosis of CTE. Tau protein is biologically defined as a protein associated with microtubule and is located within the central nervous system of the general population. Tau is found in a soluble state, and it naturally stabilizes intracellular microtubules. Ban et al. (2016) has also highlighted the proposed McKee four-stage CTE criteria that were done using the postmortem analysis done on donated athletes' brains. All stages involve a progressive increase in p tau in the affected regions. The criteria were challenged by Davis and his colleagues who interpreted stage I and II as normal aging and stage III and IV as a type of FTDL. Ban et al. (2016) state that Davis and his colleagues concluded their review by reporting that development of CTE is not linked to participating in sports.

According to Beal (2017), thoughts of committing suicide is one of the symptoms of CTE development. Wortzel, Shura, and Brenner (2013) have conducted research on the relationship between CTE and suicide. Many case reports describe suicide behaviors as one of the effects of traumatic brain injury (TBI), which is correlated to histopathology that is linked to CTE (Wortzel, Shura, & Brenner, 2013). Most of these study findings involve the connection between suicide thoughts and CTE among military veterans and athletes, resulting in widespread public concern and media attention. Wortzel, Shura, and Brenner (2013) state that most of these publications contain statements that suggest a strong relationship between suicide deaths and CTE. At least one of the CTE experts has claimed that CTE accounts for a share of these suicide deaths. 

The claim that CTE is associated with suicide deaths among footballers poses significant implications on policymaking, public health and safety, and clinical practice for professional sports organizations. Due to these implications and the people potentially at risk, Wortzel, Shura, and Brenner (2013) suggest the need for a critical review of the biological state that links CTE and suicide. According to Wortzel, Shura, and Brenner (2013), the existing histopathological findings might not provide the necessary incremental value to determine whether suicide is linked to the development of CTE. Therefore, these authors believe that more advanced research should be done to describe the association between CTE and death by suicide.

Manley et al. (2017), in his systematic analysis of possible effects of concussion-related to sports among retired athletes, established that some former players develop cognitive deficits and depression. The research also claimed that there is a connection between multiple past concussions and these deficits. However, the research also claims that former participants in sports are less likely to commit suicide. However, it was also established that those who played football in high school often experience neurodegenerative disorders later in life. Several studies concluded that retired football professionals in the U.S are predisposed to mild cognitive impairment or diminished cognitive functioning (Manley et al., 2017). One study claimed that these population is susceptible to neurodegenerative diseases. Neuroimaging reviews have established that some former players experience macrostructural, functional, neurochemical, and microstructural changes years after leaving the field. Manley et al. (2017) concluded his research by stating that more research should be done on CTE to explain its prevalence better and how this condition is associated with repetitive brain impact and concussions that are sustained during sports. 

According to McKee et al. (2013), CTE is a brain degeneration condition characterized by the piling of hyperphosphorylated tau protein in the brain. The scientists involved in this research, after a review of the disease, recommended that a minimum staining and blocking scheme is used for pathological evaluation. The study conducted by McKee and his colleagues (2016) shows that we have advanced the initial steps of validating neuropathological criteria for the development of CTE, and this gives people hope for future mechanistic and clinical studies.

Research done on the aftermath of head trauma by Senecal, Gurchiek, and Slattery (2017) revealed that there is a similar pattern of unusual deposits of proteins in the brains of retired football players who were victims of concussions. The imaging of the brains of these players found image pattern of concussions victims to be significantly different from that of those who have never experienced heat impacts. Senecal, Gurchiek, and Slattery (2017) believe that the findings of these recent studies might lead to a more convincing explanation of the brain disorders of former football players. Besides, available research would assist scientists and doctors to test treatment mechanisms and prevent progression of the disease before it causes significant symptoms and damage to the brain. 

To sum up, CTE commonly develops among military veterans, athletes, footballers, boxers, and other people involved in sports activities. Research done on CTE reveals that symptoms of the conditions include rage, bipolar, suicide thoughts, memory loss, irritability, and loss of emotional control, among other cognitive dysfunction characteristics. The relationship between CTE and suicide among players was also a research topic, and it showed that the condition might lead to suicidal through among victims. Among football players, predisposing factors include the age of exposure, the presence of the Apoε4 protein allele in the brain (genetic susceptibility), and repetitive head trauma. There is no living diagnosis of CTE; it can only be diagnosed during postmortem. Besides, there are no treatments and control mechanisms that can help prevent progression or cure the disease. The current literature review shows that there are still gaps in CTE research among football players. Current published work does not have sufficient information on how the condition occurs and its symptoms. However, research indicates that there is hope for a living diagnostic mechanism and maybe treatments in the future.

References

Ban, V. S., Madden, J., Christopher, B. E., Batjer, H., & Lonser, R. R. (2016). The Science and Questions Surrounding Chronic Traumatic Encephalopathy. Neurosurgical Focus, 40(4), 1-10.

Baugh, M. C., Robbins, A. C., Stern, A. R., & McKee, C. A. (2014). Current Understanding of Chronic Traumatic Encephalopathy. Current Treatment Options in Neurology, 16(9), 306. 

Beal, A. Judy. (2017). The Dangers of Youth Football. The American Journal of Maternal/Child Nursing, 42(6), 361.

Manley, G., Gardner, J. A., Schneider, J. K., Guskiewicz, M. K., Bailes, J., Cantu, C. R., Castellani, J. R., Turner, M., Jordan, D. B., Randolph, C., Iverson, L. G., Tator, H. C., Hayden, K. A., Dvorak, J., & McCrory, P. (2017). A Systematic Review of Potential Long-Term Effects of Sport-Related Concussion. British Journal of Sports Medicine, 51(12), 969-977.

Maroon, C. J., Winkleman R., Bost J., Amos A., Mathyssek C., & Miele, V. (2015). Chronic Traumatic Encephalopathy in Contact Sports: A Systematic Review of All Reported Pathological Cases. PLOS ONE, 10(2).

McKee, C. A., Cantu, C. R., Nowinski, J. C., Hedley-Whyte, E. T., Gavett, E. B., Budson, E. A., Santini, E. V., Lee, H., Kubilus, A. C., & Stern, A. R. (2016). Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy Following Repetitive Head Injury. Journal of Neuropathology and Experimental Neurology, 68(7), 709-735.

McKee, A. C., Stern, R. A., Nowinski C. J., et al. (2013). The Spectrum of Disease in Chronic Traumatic Encephalopathy. Brain, 136(1), 43-64. 

Senecal, G., Gurchiek, E., & Slattery, E. (2017). The Brain and Beyond in the Aftermath of Head Trauma-A Systems View of Development for Contact Sport Athletes. Cogent Psychology, 4(1).

Tharmaratnam, T., Iskandar, A. M., Tabobondung, C. T., Tobbia, I., Goee-Ramanan, P., & Tabobondung, A. T. (2018). Chronic Traumatic Encephalopathy in Professional American Football Players: Where Are We Now? Frontiers in Neurology, 9, 445.

Wortzel, S. H., Shura, D. R., & Brenner, A. L. (2013). Chronic Traumatic Encephalopathy and Suicide: A Systematic Review. Biomed Research International, 2013.