In the largest autopsy study to date of American football players, 177, or 87 percent, of the brains of 202 former players who had donated them for research showed evidence of chronic traumatic encephalopathy (CTE), a neurodegenerative condition associated with repeated blows to the head and tau deposition. In the study, 110 of 111 ex-players in the National Football League had CTE. The disease came with mood, behavior, and cognitive problems and, in severe cases, dementia. The study, from Ann McKee and colleagues at Boston University School of Medicine, appeared in the July 25 issue of JAMA.
The authors do not claim that most football players will get CTE. The brain donors are a select group whose families chose to participate in the brain bank, and are not necessarily representative of players as a whole. However, the study strengthens the link between repetitive hits to the head in football and later CTE, at least in some players.
The startling numbers should be a call to action, McKee told Alzforum. “Let’s stop quibbling about whether or not there’s a problem. Let’s get together and actually do something about it,” she said.
The new study draws on a brain bank established by McKee and colleagues to study the neuropathological consequences of repetitive head trauma in athletes and soldiers. Most of the men in the new study had played in high school or college, or at the professional level. The median age of death was 67, and they played for an average of 15 years. CTE was classified as mild or severe, based on recently published pathological criteria (McKee et al., 2016). Extensive interviews with family and friends provided a detailed picture of symptoms and clinical progression.
In total, 177 cases merited a neuropathological diagnosis of CTE. Either mild or severe pathology produced frequent mood, behavior and cognitive, symptoms. Most of the severe cases, which included the majority of former college and professional players, also developed dementia. There were no cases of asymptomatic CTE pathology.
In its mildest form, tau pathology appeared as a few focal lesions restricted to the cortex. Yet, even subjects with this circumscribed pathology showed severe symptoms, McKee and colleagues found. That suggests other as-yet unexamined pathologies could account for some of the manifestations of CTE in this group. They include axonal pathology (Jan 2013 news), white matter changes, or inflammation (Dec 2016 news). The BU CTE brain bank, which makes tissue available to researchers, is a unique resource McKee hopes will encourage additional investigators to study these possibilities.
Comorbidities were common: 91 percent of cases with the most severe stage IV CTE also had amyloid, 83 percent had TDP-43 deposits, and 43 percent had α-synuclein. The development of other pathologies is age-related, said McKee, and raises the possibility that repetitive brain injury or CTE is a risk factor for multiple neurodegenerative diseases.
McKee’s group is continuing to collect cases. Going forward, the researchers will focus on risk factors. Is how long a player’s career lasted important, or the age when he started, or the position he played? McKee told Alzforum she is looking at other environmental factors such as substance use, steroids, and cardiovascular risk. By now her team has a large enough sample to start to pursue genetics, too.—Pat McCaffrey
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- Rabinovici GD. Advances and Gaps in Understanding Chronic Traumatic Encephalopathy: From Pugilists to American Football Players. JAMA. 2017 Jul 25;318(4):338-340. PubMed.