Oxidative Stress-Driven Deficits in Animal Models of Neurotrauma
Abstract
Traumatic injuries are the leading cause of loss of human potential worldwide, killing nearly 5 million people a year. Within this broad category, injuries to the central nervous system (CNS); spinal cord injury (SCI) and traumatic brain injury (TBI), are the most prevalent and with the highest economic cost to society. The damage from these initial mechanical insults is exacerbated by distinct but interconnected secondary mechanisms. Nervous tissue is especially sensitive to the detrimental effects of oxidative stress mainly due to its high energy needs and high lipid content, which makes it more vulnerable to oxidants. The lipid peroxidation by-product, acrolein is a well-known oxidant and proinflammatory cytotoxin with a stronger self-perpetuating nature than most other oxidative agents. Acrolein has been widely implicated in disease progression and is an ideal target for therapeutic intervention. Thus, we have correlated acrolein levels and acrolein-mediated pathologies to behavioral deficits after acute forms of spinal cord injury (SCI) and mild blast-induced traumatic brain injury (mbTBI) in rats.
Degree
Ph.D.
Advisors
Shi, Purdue University.
Subject Area
Neurosciences
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