Chronic Traumatic Encephalopathy: The cellular sequela to repetitive brain injury.

Citation data:

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia, ISSN: 1532-2653, Vol: 41, Page: 24-29

Publication Year:
2017
Usage 154
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PMID:
28347679
DOI:
10.1016/j.jocn.2017.03.035
Author(s):
Vile, Alexander R; Atkinson, Leigh
Publisher(s):
Elsevier BV
Tags:
Neuroscience; Medicine
review description
This review aims to integrate current literature on the pathogenic mechanisms of Chronic Traumatic Encephalopathy (CTE) to create a multifactorial understanding of the disease. CTE is a progressive neurodegenerative disease, classed as a tauopathy, although it appears the pathogenic mechanisms are more complex than this. It affects those with a history of repetitive mild traumatic brain injury. Currently, there are no treatments for CTE and the disease can only be affirmatively diagnosed in post mortem. Understanding the pathogenesis of the disease will provide an avenue to explore possible treatment and diagnostic modalities. The pathological hallmarks of CTE have been well characterised and have been linked to the pathophysiologic mechanisms in this review. Human studies are limited due to ethical implications of exposing subjects to head trauma. Phosphorylation of tau, microglial activation, TAR DNA-binding protein 43 and diffuse axonal injury have all been implicated in the pathogenesis of CTE. The neuronal loss and axonal dysfunction mediated by these pathognomonic mechanisms lead to the broad psycho-cognitive symptoms seen in CTE.