There has been a lot of publicity over the last year about the links between neurodegenerative disease and multiple mild head injuries incurred in many common sports including football and rugby, for example Alan Shearer's BBC documentary on the links between dementia and football. Chronic traumatic encephalopathy (CTE) is a term that has been coined to describe patients who develop behavioural, mood, cognitive and motor disturbances after prolonged exposure to mild head injuries and show abnormal protein folding in the brain.
Alan Shearer, footballer (from the BBC documentary Alan Shearer: Dementia, Football and Me) https://www.bbc.co.uk/programmes/b09g0gzk)
This disease process bears similarities to Parkinson's Disease in that normal proteins become misfolded and then aggregate into abnormal deposits which is then associated with brain cell death. We have also known for a long time that previous history of head injuries and concussion increases your risk of Parkinson's. The study below, of almost 700 individuals including a significant number of athletes who had died and agreed to have an autopsy looks in more detail at the links between these conditions.
Overall, they found that people who had repeated head injury during life were much more likely to have the abnormal protein found in Parkinson's, alpha-synuclein, as well as the tau protein, which has been described in CTE. More exposure to head injury - for example greater than 8 years of playing contact sport increased the likelihood of Parkinson's-type pathology. They go on to look at the relationships between the different forms of protein and show that the distribution of the Parkinson's protein alpha-synculein is similar whether or not there was evidence of CTE and likely accounts for the movement problems seen in CTE.
Descriptions of protein-related brain diseases are ever expanding and I believe will guide us in understanding the causes of Parkinson's and how the disease progresses. By studying the processes by which mild head injury leads to protein misfolding and how the different proteins interact we are gaining new mechanistic insights which we hope will lead to promising new treatments. From a prevention point of view, the neurological dangers of repetitive mild head injury are increasingly clear - while the authors here showed that playing more than 8 years of competitive sport was significantly associated with more pathology, we still need more data before we can develop clear recommendations for both our patients and the wider public.
-Anna
https://academic.oup.com/jnen/advance-article/doi/10.1093/jnen/nly065/5059623
Alan Shearer, footballer (from the BBC documentary Alan Shearer: Dementia, Football and Me) https://www.bbc.co.uk/programmes/b09g0gzk)
This disease process bears similarities to Parkinson's Disease in that normal proteins become misfolded and then aggregate into abnormal deposits which is then associated with brain cell death. We have also known for a long time that previous history of head injuries and concussion increases your risk of Parkinson's. The study below, of almost 700 individuals including a significant number of athletes who had died and agreed to have an autopsy looks in more detail at the links between these conditions.
Overall, they found that people who had repeated head injury during life were much more likely to have the abnormal protein found in Parkinson's, alpha-synuclein, as well as the tau protein, which has been described in CTE. More exposure to head injury - for example greater than 8 years of playing contact sport increased the likelihood of Parkinson's-type pathology. They go on to look at the relationships between the different forms of protein and show that the distribution of the Parkinson's protein alpha-synculein is similar whether or not there was evidence of CTE and likely accounts for the movement problems seen in CTE.
Descriptions of protein-related brain diseases are ever expanding and I believe will guide us in understanding the causes of Parkinson's and how the disease progresses. By studying the processes by which mild head injury leads to protein misfolding and how the different proteins interact we are gaining new mechanistic insights which we hope will lead to promising new treatments. From a prevention point of view, the neurological dangers of repetitive mild head injury are increasingly clear - while the authors here showed that playing more than 8 years of competitive sport was significantly associated with more pathology, we still need more data before we can develop clear recommendations for both our patients and the wider public.
-Anna
https://academic.oup.com/jnen/advance-article/doi/10.1093/jnen/nly065/5059623
Lewy Body Pathology and Chronic Traumatic Encephalopathy Associated With Contact Sports.
Adams JW, Alvarez VE, Mez J, Huber BR, Tripodis Y, Xia W, Meng G, Kubilus CA, Cormier K, Kiernan PT, Daneshvar DH, Chua AS, Svirsky S, Nicks R, Abdolmohammadi B, Evers L, Solomon TM, Cherry JD, Aytan N, Mahar I, Devine S, Auerbach S, Alosco ML, Nowinski CJ, Kowall NW, Goldstein LE, Dwyer B, Katz DI, Cantu RC, Stern RA, Au R, McKee AC, Stein TD
Traumatic brain injury has been associated with increased risk of Parkinson disease and parkinsonism, and parkinsonism and Lewy body disease (LBD) can occur with chronic traumatic encephalopathy (CTE). 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). 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 ɛ4 allele status. Clinically, dementia was significantly associated with neocortical LBD, CTE stage, and AD; parkinsonism was associated with LBD pathology but not CTE stage. Contact sports participation may increase risk of developing neocortical LBD, and increased LBD frequency may partially explain extrapyramidal motor symptoms sometimes observed in CTE.
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