Citation

Kim S, Han SC, Gallan AJ, Hayes JP. Concussion 2017; 2(3): CNC48.

Affiliation

Department of Psychiatry, Boston University School of Medicine, Boston, MA 02118, USA.

Copyright

(Copyright © 2017, The Drake Foundation, Publisher Future Medicine)

DOI

10.2217/cnc-2017-0013

PMID

30202587

PMCID

PMC6128012

Abstract

Mild traumatic brain injury (mTBI) is a significant national health concern and there is growing evidence that repetitive mTBI (rmTBI) can cause long-term change in brain structure and function. The mitochondrion has been suggested to be involved in the mechanism of TBI. There are noninvasive methods of determining mitochondrial dysfunction through biomarkers and spectroscopy. Mitochondrial dysfunction has been implicated in a variety of neurological consequences secondary to rmTBI through activation of caspases and calpains. The purpose of this review is to examine the mechanism of mitochondrial dysfunction in rmTBI and its downstream effects on neuronal cell death, axonal injury and blood-brain barrier compromise.

Language: en

Keywords

TBI; axonal injury; biomarkers; blood–brain barrier; mTBI; mitochondrial dysfunction; rmTBI