• Cold Spring Harb Perspect Med · Feb 2018

    Review

    Chronic Traumatic Encephalopathy: Is Latency in Symptom Onset Explained by Tau Propagation?

    • Joshua Kriegel, Zachary Papadopoulos, and Ann C McKee.
    • Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, Massachusetts 02118.
    • Cold Spring Harb Perspect Med. 2018 Feb 1; 8 (2).

    AbstractChronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive mild brain trauma. CTE, previously termed "dementia pugilistica," has been identified in American football, ice hockey, baseball, rugby and soccer players, boxers, wrestlers, and military personnel exposed to blast and other traumatic brain injuries. There is often a long latency period between an individual's exposure to repetitive brain trauma and the clinical symptoms of CTE. The pathology of CTE is characterized by a progression from isolated focal perivascular hyperphosphorylated tau lesions in the cerebral cortex to a widespread tauopathy that involves diffuse cortical and medial temporal lobe regions. We hypothesize that the spread of tau from focal perivascular lesions to a widespread tauopathy occurs as a result of intraneuronal and intrasynaptic prion-like protein templating, as well as tau secretion and propagation along glymphatic and cerebrospinal fluid pathways.Copyright © 2018 Cold Spring Harbor Laboratory Press; all rights reserved.

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