Blast injury-induced neurotrauma (BINT) is steadily increasing in prevalence due to escalated terror activity and constitutes the signature injury associated with current military conflicts. BINT produces significant neurological deficiencies and there is a growing concern that the injury may produce long-term consequences that affect the resilience and the performance of soldiers. One of the potential consequences is an increased susceptibility to Parkinson's disease (PD). A vital goal aimed at curtailing the post-deployment long-term consequences of blast injury-induced neurotrauma is to further our knowledge of pathogenic mechanisms responsible for the escalation of post injury diseases. The purpose of this project is to investigate the molecular mechanism underlying the susceptibility of PD in post-blast rats. We have identified acrolein, a highly reactive aldehyde that persists days to weeks following brain-injury and perpetuates oxidative insult, as a potential therapeutic target to curtail chemically mediated damage, a common feature of BINT and PD. Our hypothesis is that acrolein is a key pathological factor linking BINT and the development of PD in our rat model.
|Commitee:||Rochet, Chris, Suter, Daniel|
|Department:||PULSe (Life Sciences)|
|School Location:||United States -- Indiana|
|Source:||MAI 54/02M(E), Masters Abstracts International|
|Subjects:||Molecular biology, Neurosciences|
|Keywords:||Blast, Parkinson's disease, Traumatic brain injury|
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