You mean that repeated hits to the head might lead to long term brain damage?
Gee. What a revelation.
In context, it also leads to a hefty bank balance. Cost-benefit analysis
Research on CTE has advanced considerably over the past five years, and the BU CTE Center soon will publish its 182nd study on CTE. In part because of advances in research on CTE, in October 2022 the National Institutes of Neurological Disorders and Stroke (NINDS), a branch of the National Institutes of Health (NIH), updated their position on what causes CTE: “CTE is a delayed neurodegenerative disorder that was initially identified in postmortem brains and, research-to-date suggests, is caused in part by repeated traumatic brain injuries.”
CTE is a progressive neurodegenerative disease frequently found in contact sports athletes. However, many former contact sports athletes suffer from thinking problems and impulsive behavior in the absence of CTE, or with very mild CTE. This new study suggests that a separate type of brain damage, which can appear earlier than CTE, may underlie some of these symptoms.
“Damage to the white matter may help explain why football players appear more likely to develop cognitive and behavioral problems later in life, even in the absence of CTE,” said corresponding author Thor Stein, MD, PhD, a neuropathologist at VA Boston Healthcare System and assistant professor of pathology and laboratory medicine at Boston University Chobanian & Avedisian School of Medicine.
The researchers studied the brains of 205 deceased American football players donated to the Veterans Affairs-Boston University-Concussion Legacy Foundation (VA-BU-CLF) Brain Bank and measured levels of myelin, a component of white matter that covers, protects and speeds up the connections in the brain. They then interviewed family members on measures of cognition and impulsivity and then compared how career length and age of beginning tackle football related to levels of myelin, and how myelin levels related to cognition and impulsivity. In addition to more years of football played, the researchers found that starting tackle football at a younger age was also related to more white matter loss, independent of career length.
The brains of people who die with CTE are marked by the accumulation of a protein called tau, the same protein found to aggregate in Alzheimer’s disease (AD) brain. The amount of tau pathology in CTE correlates with severity of disease, where early-stage brains have very little pathology and late stage show severe, widespread involvement. The amount of RHI exposure, which for athletes can be measured in terms of the number of years they played a violent sport, as well as genetic risk variants influence the extent of tau pathology and associated disease severity. However, the molecular and genetic mechanisms that underly the development disease, and to what extent those effects are consistent throughout disease progression, are poorly understood.
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The researchers generated gene expression data for each individual and then performed bioinformatic and statistical analyses of the different subsets of these samples to look for gene expression patterns that are associated with different clinical, histological and genetic markers that are relevant to CTE. They then identified genes and biological processes associated with total years of play as a measure of exposure, amount of tau pathology present at time of death, and the presence of APOE and TMEM106B risk variants.
The researchers found substantial gene expression changes were associated with severe disease for most of these factors, primarily implicating diverse, strongly involved neuro-inflammatory and neuro-immune processes. In contrast, low pathology groups had many fewer gene expression changes and neuroimmune or inflammatory processes implicated and showed striking differences for some factors when compared with severe disease.
According to the researchers, if the active disease process in early disease differs substantially from late-stage disease, this could have important implications for both diagnostic and therapeutic targets. “This might explain why therapeutic targets identified from late-stage human tissue have largely failed to influence disease progression in clinical trials for many neurodegenerative diseases. In addition, if there are distinct markers of early disease progression that are absent in late disease, this would provide an opportunity to explore different diagnostics and biomarkers that we otherwise wouldn’t know to look for,” explained co-corresponding author Thor Stein, MD, PhD, a neuropathologist at VA Boston Healthcare System and associate professor of pathology and laboratory medicine.