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Int. J. Mol. Sci. 2017, 18(12), 2600; doi:10.3390/ijms18122600

Diffuse Axonal Injury and Oxidative Stress: A Comprehensive Review

1
Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Neuromed, Via Atinense 18, 86077 Pozzilli, Italy
2
Department of Neurosciences, Mental Health, and Sensory Organs, Sant’Andrea Hospital, Sapienza University of Rome, Via di Grottarossa 1035, 00189 Rome, Italy
3
Department of Medicine, Surgery and Neuroscience, University of Siena, Viale Mario Bracci 16, 53100 Siena, Italy
4
Department of Anatomical, Histological, Forensic and Orthopaedic Sciences, Sapienza University of Rome, Viale Regina Elena 336, 00185 Rome, Italy
*
Author to whom correspondence should be addressed.
Received: 16 September 2017 / Revised: 17 November 2017 / Accepted: 28 November 2017 / Published: 2 December 2017
(This article belongs to the Special Issue Neuroprotective Strategies 2017)
View Full-Text   |   Download PDF [2653 KB, uploaded 2 December 2017]   |  

Abstract

Traumatic brain injury (TBI) is one of the world’s leading causes of morbidity and mortality among young individuals. TBI applies powerful rotational and translational forces to the brain parenchyma, which results in a traumatic diffuse axonal injury (DAI) responsible for brain swelling and neuronal death. Following TBI, axonal degeneration has been identified as a progressive process that starts with disrupted axonal transport causing axonal swelling, followed by secondary axonal disconnection and Wallerian degeneration. These modifications in the axonal cytoskeleton interrupt the axoplasmic transport mechanisms, causing the gradual gathering of transport products so as to generate axonal swellings and modifications in neuronal homeostasis. Oxidative stress with consequent impairment of endogenous antioxidant defense mechanisms plays a significant role in the secondary events leading to neuronal death. Studies support the role of an altered axonal calcium homeostasis as a mechanism in the secondary damage of axon, and suggest that calcium channel blocker can alleviate the secondary damage, as well as other mechanisms implied in the secondary injury, and could be targeted as a candidate for therapeutic approaches. Reactive oxygen species (ROS)-mediated axonal degeneration is mainly caused by extracellular Ca2+. Increases in the defense mechanisms through the use of exogenous antioxidants may be neuroprotective, particularly if they are given within the neuroprotective time window. A promising potential therapeutic target for DAI is to directly address mitochondria-related injury or to modulate energetic axonal energy failure. View Full-Text
Keywords: traumatic brain injury; oxidative stress; reactive oxygen species; immunohistochemistry; biomarkers traumatic brain injury; oxidative stress; reactive oxygen species; immunohistochemistry; biomarkers
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Frati, A.; Cerretani, D.; Fiaschi, A.I.; Frati, P.; Gatto, V.; La Russa, R.; Pesce, A.; Pinchi, E.; Santurro, A.; Fraschetti, F.; Fineschi, V. Diffuse Axonal Injury and Oxidative Stress: A Comprehensive Review. Int. J. Mol. Sci. 2017, 18, 2600.

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