Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by a distinct deposition of hyperphosphorylated tau (p-tau) in a pattern that is unique from other diseases including Alzheimer disease.1,2 The pathognomonic lesions of CTE include perivascular accumulation of p-tau in neurons, astrocytes, and cell processes at the depths of the cortical sulci.2 Amyloid-β peptide (Aβ) deposition, either as diffuse or neuritic plaques, has been found to be present in approximately half of postmortem CTE cases; however, when present in CTE, Aβ deposition is associated with accelerated neuropathological and clinical progression of CTE.3 Chronic traumatic encephalopathy is also associated with variable transactive response DNA-binding protein 43 pathology as well as axonal degeneration, white matter degradation, neuroinflammation, and neuronal loss, suggesting that CTE involves a complex polypathology with p-tau deposition as a constant.4 Chronic traumatic encephalopathy has been found most often in professional contact sport athletes who have been subjected to repetitive head impacts (RHI) resulting in concussive and subconcussive trauma, eg, boxers and American football players.5 However, a 2015 study in a large neurodegenerative disorders brain bank found CTE neuropathology in approximately one-third of former amateur contact sports athletes.6 Neuropathologically confirmed CTE has also been found in nonathletes with RHI exposure including individuals with epilepsy, survivors of physical abuse, and military service members.1
Stern RA. Cerebrospinal Fluid Biomarkers in Postconcussion Syndrome: Measuring Neuronal Injury and Distinguishing Individuals at Risk for Persistent Postconcussion Syndrome or Chronic Traumatic Encephalopathy. JAMA Neurol. 2016;73(11):1280–1282. doi:10.1001/jamaneurol.2016.3169
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