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Parkinson's Symptoms Associated with Contact Sports

2018-07-27
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In recent years awareness about the neurological risks associated with playing contact sports has risen exponentially. This increased mindfulness stems from the mounting evidence that repetitive head impacts from contact sports and other exposures are associated with the neurodegenerative disease chronic traumatic encephalopathy (CTE) and dementia.

Now, new data from a team of investigators at Boston University (BU) suggests that contact sports athletes may also be at increased risk for Lewy Body Disease (LBD), which can cause Parkinson’s disease.

The findings from the new study, published recently in the Journal of Neuropathology and Experimental Neurology through an article titled “Lewy Body Pathology and Chronic Traumatic Encephalopathy Associated With Contact Sports,” suggest that LBD causes the motor disorders that appear in a minority of CTE cases, including tremors, slowness, and difficulty walking.

Parkinson's-Symptoms.jpg

“We found the number of years an individual was exposed to contact sports, including football, ice hockey, and boxing, was associated with the development of neocortical LBD, and LBD, in turn, was associated with parkinsonism and dementia,” explains senior study investigator Thor Stein, M.D., Ph.D., a neuropathologist at VA Boston Healthcare System and assistant professor of pathology and laboratory medicine at Boston University School of Medicine (BUSM).

LBD, which can lead to Parkinson’s disease and Lewy body dementia, is associated with problems with movement, cognition, depression, sleep, and visual hallucinations. This newfound relationship between contact sports and LBD appears to be independent of CTE pathology.

In the current study, the research team examined 694 brains from three repositories, including the Veteran’s Affairs-Boston University-Concussion Legacy Foundation (VA-BU-CLF) Brain Bank, BU Alzheimer’s Disease Center, and the Framingham Heart Study.

“To test whether contact sports and CTE are associated with LBD, we compared deceased contact sports athletes (n = 269) to cohorts from the community (n = 164) and the Boston University Alzheimer disease (AD) Center (n = 261),” the authors wrote. “Participants with CTE and LBD were more likely to have β-amyloid deposition, dementia, and parkinsonism than CTE alone (p < 0.05). Traditional and hierarchical clustering showed a similar pattern of LBD distribution in CTE compared to LBD alone that was most frequently neocortical, limbic, or brainstem. In the community-based cohort, years of contact sports play were associated with neocortical LBD (OR = 1.30 per year, p = 0.012), and in a pooled analysis a threshold of >8 years of play best predicted neocortical LBD (ROC analysis, OR = 6.24, 95% CI = 1.5–25, p = 0.011), adjusting for age, sex, and APOE? 4 allele status.”

Interestingly, the total years of contact sports play was linked to an increased risk of having LBD in the cortex of the brain. Those who played more than eight years of contact sports had the greatest risk of LBD, which was six times higher than those who played eight years or less. Clinically, athletes with both CTE and LBD were significantly more likely to have dementia and the symptoms of Parkinson’s disease than those with CTE pathology alone.

The researchers had previously shown that other brain changes are correlated with the total years of contact sports play. In prior studies, the number of years of tackle football participation was found to predict the severity of tau pathology in the dorsolateral frontal cortex and as well as CTE stage. Additionally, individuals with a history of repetitive head impacts and neuropathological diagnosis of CTE accumulate beta-amyloid (Aβ) at a younger age and an accelerated rate compared to controls. The research builds upon previous research from other groups showing an association between concussion/traumatic brain injury and Parkinson’s disease.

This new study advances our understanding of the consequences of repetitive head impacts in contact sports on the development of clinical symptoms and the pathology that underlies them. The researchers are committed to continuing their research as they are they are keenly aware that further work is essential to define better the risks associated with repetitive head impacts and neurodegeneration.

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