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Citation |
Wong VS, Langley B. Neurosci. Lett. 2016; 625: 26-33. |
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Affiliation |
Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, United States; Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 E. 68th Street, New York, NY 10065, United States. Electronic address: bcl2002@med.cornell.edu. |
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Copyright |
(Copyright © 2016, Elsevier Publishing) |
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DOI |
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PMID |
27155457 |
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Abstract |
Traumatic brain injury (TBI) contributes to nearly a third of all injury-related deaths in the United States. For survivors of TBI, depending on severity, patients can be left with devastating neurological disabilities that include impaired cognition or memory, movement, sensation, or emotional function. Despite the efforts to identify novel therapeutics, the only strategy to combat TBI is risk reduction (helmets, seatbelts, removal of fall hazards, etc.). Enormous heterogeneity exists within TBI, and it depends on the severity, the location, and whether the injury was focal or diffuse. Evidence from recent studies support the involvement of epigenetic mechanisms such as DNA methylation, chromatin post-translational modification, and miRNA regulation of gene expression in the post-injured brain. In this review, we discuss studies that have assessed epigenetic changes and mechanisms following TBI, how epigenetic changes might not only be limited to the nucleus but also impact the mitochondria, and the implications of these changes with regard to TBI recovery. Language: en |