Nanoparticle Treatment to Counter Reactive Oxygen Species after Traumatic Brain Injury

Authors

Brandon McDonald, University of Nebraska - LincolnFollow
Forrest Kievit, University of Nebraska - LincolnFollow

Date of this Version

4-2020

Document Type

Poster

Citation

McDonald, B. & Kievit, F. (2020, April). Nanoparticle Treatment to Counter Reactive Oxygen Species after Traumatic Brain Injury. Poster presentation, UCARE Research Fair, Spring 2020, University of Nebraska-Lincoln.

Comments

Copyright 2020 by the authors.

Abstract

Traumatic brain injury (TBI) is defined as damage to the brain, resulting from an external mechanical force, such as an impact to the head (Kievit et. al, 2016).There are several examples that could result in a potential TBI; such as falling with contact to the head, car accidents and even physical activities including football, wrestling, and boxing. Because of the several different scenarios that an individual could impact their head, TBI’s have become an all too common aspect of everyday life. TBI is currently the leading cause of death and disability in children and adults under the age of 45, with 1.7 million reported cases annually in the United States alone(Bharadwaj et. al, 2016). The major problem that causes TBIs to be so lethal is the combination of both the initial damage and the secondary corrosive damage on the surrounding brain tissue. The initial damage is capable of being prevented by wearing helmets, seat belts and taking other safety precautions. However, there are currently no treatments that protect the brain from secondary deterioration, spread of the injury beyond primary damage (Kievit et. al, 2016). While some individuals are capable of fully recovering from a TBI without secondary brain damage, unfortunately, roughly 35% of TBI survivors face long-term disabilities (McConeghy et. al, 2012). The lethal progression of this secondary injury is in part caused by the release of reactive oxygen species (ROS) into the surroundings of the normal brain (Kievit et. al, 2016). From this information, it seems that the best way to prevent this secondary spread to the brain would be to reduce or eliminate the spread of ROS. In order to control this release of ROS, there must be a chemical, or biological entity, placed into the brain that reacts with these ROS so that they are incapable of reacting with the healthy portions of the brain. Currently, Dr. Kievit’s lab is developing nanoparticles that can react with these ROS and prevent them from spreading into other areas of the brain.