Citation

Nagalakshmi B, Sagarkar S, Sakharkar AJ. Prog. Mol. Biol. Transl. Sci. 2018; 157: 263-298.

Affiliation

Savitribai Phule Pune University, Pune, Maharashtra, India. Electronic address: amul.sakharkar@unipune.ac.in.

Copyright

(Copyright © 2018, Elsevier Publishing)

DOI

10.1016/bs.pmbts.2017.12.013

PMID

29933953

Abstract

Of all types of injuries, traumatic brain injuries (TBIs) are most likely to result in death or permanent physical or mental disabilities. With the increased frequency of military operations, terror attacks, sports activities, and road mishaps, TBIs are increasingly becoming a serious public health concern. Patients who meet with moderate-to-severe TBI suffer from a constellation of cognitive deficits and phenotypes due to diffuse axonal injury. On the contrary, minimal TBI precipitates in long-term behavioral complications commonly referred to as post-traumatic stress disorders, which consist of depression, anxiety, hallucinations, and so on. During the last decade, epigenetic mechanisms, such as histone posttranslational modifications, DNA methylation, and noncoding RNAs, have received reasonable attention by scientists studying the neurobiology of TBI. Chromatin remodeling sculpted by various epigenetic factors in different parts of the brain controls many intricate processes involved in important neural functions. Although stable and dogmatic, the reversible nature of epigenetic modifications has attracted special attention for their emerging potential in therapeutic development. Herein, we offer an overview of recent observations on epigenetic pathways that are likely involved in shaping neural function and maintain the state of neuropathology in response to traumatic events.

Copyright © 2018. Published by Elsevier Inc.

Language: en

Keywords

DNA methylation; DNMT; anxiety; chromatin remodeling; histone acetylation; microRNA; post-traumatic stress disorders; traumatic brain injury