Journal
ANNUAL REVIEW OF PATHOLOGY: MECHANISMS OF DISEASE, VOL 11
Volume 11, Issue -, Pages 21-45Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-pathol-012615-044116
Keywords
traumatic brain injury; CTE; neurodegeneration; axons; tau; amyloid
Categories
Funding
- NIA NIH HHS [R03 AG038911] Funding Source: Medline
- NINDS NIH HHS [R01 NS038104, R01 NS092398, P01 NS056202, R01 NS094003] Funding Source: Medline
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Almost a century ago, the first clinical account of the punch-drunk syndrome emerged, describing chronic neurological and neuropsychiatric sequelae occurring in former boxers. Thereafter, throughout the twentieth century, further reports added to our understanding of the neuropathological consequences of a career in boxing, leading to descriptions of a distinct neurodegenerative pathology, termed dementia pugilistica. During the past decade, growing recognition of this pathology in autopsy studies of non-boxers who were exposed to repetitive, mild traumatic brain injury, or to a single, moderate or severe traumatic brain injury, has led to an awareness that it is exposure to traumatic brain injury that carries with it a risk of this neurodegenerative disease, not the sport or the circumstance in which the injury is sustained. Furthermore, the neuropathology of the neurodegeneration that occurs after traumatic brain injury, now termed chronic traumatic encephalopathy, is acknowledged as being a complex, mixed, but distinctive pathology, the detail of which is reviewed in this article.
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