Abstract

Chronic traumatic encephalopathy is a form of tauopathy that develops after minor trauma to the brain occurs repeatedly. We found indications of chronic traumatic encephalopathy in 68 out of 85 persons whose postmortem brains we examined, all of whom had histories of recurrent mild TBI. There were a total of 64 athletes, 21 veterans (86% of whom were also athletes), and one individual with a history of self-harming head banging; their ages ranged from 17 to 98 (mean 59.5). Eighteen participants of similar ages and sexes who had never experienced moderate traumatic brain injury were utilised as controls. Hyper phosphorylated tau pathology in chronic traumatic encephalopathy progressed from mild to severe, from localised perivascular epicentres of neurofibrillary tangles in the frontal neocortex to widespread tauopathy impacting several brain regions, including the medial temporal lobe. At all stages of chronic traumatic encephalopathy, multifocal axonal varicosities and axonal loss were discovered in deep cortex and subcortical white matter. DNA-binding protein TAR In 85% of the cases, there were also 43 immunoreactive inclusions and neurites, ranging from focal disease in stages I through III to extensive inclusions and neurites in stage IV. Stage I chronic traumatic encephalopathy was characterised by symptoms such as headache and inability to focus. Additional symptoms in stage II were hopelessness, impulsivity, and memory loss. Both executive dysfunction and cognitive decline characterised stage III, while dementia, difficulty communicating, and irritability characterised stage IV. Sports-related exposure data was available for 34 American football players; the stage of chronic traumatic encephalopathy was associated with greater football playing time, greater post-football survival, and greater age at death.43 individuals (63%) had a single diagnostic of chronic traumatic encephalopathy; eight had a second diagnosis of motor neuron disease (12%), seven had Alzheimer's disease (11%), 11 had Lewy body disease (16%), and four had frontotemporal lobar degeneration (6%).