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Review
. 2017 Oct 4;2(3):CNC48.
doi: 10.2217/cnc-2017-0013. eCollection 2017 Nov.

Neurometabolic indicators of mitochondrial dysfunction in repetitive mild traumatic brain injury

Susan Kim  1   1 , Steve C Han  1   1 , Alexander J Gallan  2   2 , Jasmeet P Hayes  3   4   3   4
Affiliations
Review

Neurometabolic indicators of mitochondrial dysfunction in repetitive mild traumatic brain injury

Susan Kim et al. Concussion. .

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.

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

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Conflict of interest statement

Financial & competing interests disclosure Support for this research was provided by VA SPiRe award I21RX001594 (J Hayes). The authors have no other relevant affiliations for financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript

Figures

<b>Figure 1.</b>
Figure 1.. The process of mitochondrial impairment secondary to disruption of Ca2+ homeostasis and opening of permeability transition pore.
PTP: Permeability transition pore.
<b>Figure 2.</b>
Figure 2.. The mechanism of apoptosis secondary to release of cytochrome C from the mitochondria and the resulting activation of caspases.
<b>Figure 3.</b>
Figure 3.. A schematic of blood–brain barrier and capillary in the brain.
Structures boxed in blue are components of the BBB. BBB: Blood–brain barrier.
<b>Figure 4.</b>
Figure 4.. A schematic of a disrupted blood–brain barrier.
The end results of the BBB impairment are: the disruption of tight junctions that hold together the endothelial cells of the blood vessels, the gradation of basement membrane and the impairment of pericytes and the edematous astrocytic feet that are parts of the perivascular component crucial for the integrity of BBB. BBB: Blood–brain barrier.
See this image and copyright information in PMC

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