Citation

McKee AC, Stein TD, Kiernan PT, Alvarez VE. Brain Pathol. 2015; 25(3): 350-364.

Affiliation

VA Boston Healthcare System, Boston University, Boston, MA; Department of Pathology and Laboratory Science, Boston University School of Medicine, Boston University, Boston, MA; Department of Neurology, Boston University School of Medicine, Boston University, Boston, MA; Boston University Alzheimer's Disease Center, Boston University, Boston, MA; Chronic Traumatic Encephalopathy Center Program, Boston University, Boston, MA.

Copyright

(Copyright © 2015, John Wiley and Sons)

DOI

10.1111/bpa.12248

PMID

25904048

PMCID

PMC4526170

Abstract

Repetitive brain trauma is associated with a progressive neurological deterioration, now termed as chronic traumatic encephalopathy (CTE). Most instances of CTE occur in association with the play of sports, but CTE has also been reported in association with blast injuries and other neurotrauma. Symptoms of CTE include behavioral and mood changes, memory loss, cognitive impairment and dementia. Like many other neurodegenerative diseases, CTE is diagnosed with certainty only by neuropathological examination of brain tissue. CTE is a tauopathy characterized by the deposition of hyperphosphorylated tau (p-tau) protein as neurofibrillary tangles, astrocytic tangles and neurites in striking clusters around small blood vessels of the cortex, typically at the sulcal depths. Severely affected cases show p-tau pathology throughout the brain. Abnormalities in phosphorylated 43 kDa TAR DNA-binding protein are found in most cases of CTE; beta-amyloid is identified in 43%, associated with age. Given the importance of sports participation and physical exercise to physical and psychological health as well as disease resilience, it is critical to identify the genetic risk factors for CTE as well as to understand how other variables, such as stress, age at exposure, gender, substance abuse and other exposures, contribute to the development of CTE.

Language: en