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Journal Article

Citation

Mateen BA, Hill CS, Biddie SC, Menon D. J. Neurotrauma 2017; 34(16): 2379-2388.

Affiliation

Addenbrooke's Hospital and University of Cambridge, Cambridge, United Kingdom of Great Britain and Northern Ireland ; dkm13@cam.ac.uk.

Copyright

(Copyright © 2017, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2017.5007

PMID

28482743

Abstract

This article reviews the literature pertinent to epigenetic changes, and in particular DNA methylation following Traumatic Brain Injury (TBI). TBI is a heterogeneous disease that is a major cause of death and long-term disability. The links between TBI and epigenetics, the process by which environmental factors alter gene expression without changing the underlying DNA sequence, is an expanding area of research that may have profound consequences for our understanding of the disease, and clinical care. There are various epigenetic changes that may occur as a direct result of TBI, including DNA methylation, histone modification, and changes in the levels of non-coding RNA. This review focuses on DNA methylation, its potential to alter the degree of injury, and the extent of recovery- including development of post-traumatic neurodegeneration, response to therapies, and the hereditable consequences of injury. The functional consequences of non-coding RNA and histone modifications are well described in the literature, but the mechanism by which these three mechanisms interact are often overlooked. Here, we briefly describe the interaction of DNA methylation with the two other key epigenetic changes, and highlight key work being done to understand the functional relevance of those mechanisms. The field of epigenetics is rapidly advancing due to the advent of less invasive and more versatile methods for measuring epigenetic proteins and their functional impact on cells, however, the evidence specific to TBI is limited. This review identifies several important outstanding questions that remain from the work already conducted, and highlights directions for the future.


Language: en

Keywords

ADULT BRAIN INJURY; GENOMICS; SECONDARY INSULT; TRAUMATIC BRAIN INJURY

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