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Abstract:
Chemical warfare nerve agents continue to be a threat to both military personnel and civilian populations. Organophosphorus nerve agents irreversibly inhibit the enzyme acetylcholinesterase, resulting in accumulation of high levels of the neurotransmitter acetylcholine (ACh) at muscarinic and nicotinic receptors. This accumulation of ACh induces clinical symptoms including myosis, difficulty in breathing, convulsions, seizures, and can result n death. Current medical countermeasures for treating nerve agent intoxication increase survival if administered rapidly after exposure but may not fully prevent brain injury. The downstream neurological damage induced by nerve agent exposure is not well characterized. Researchers are now utilizing molecular approaches to understand the molecular pathways involved in nerve agent-induced brain injury, with the goal of developing treatment strategies that are effective when administered after the onset of seizures and secondary responses that lead to nerve agent-induced brain injury.
| Limitations: |
 APPROVED FOR PUBLIC RELEASE |
| Description: |
Book chapter |
| Pages: |
1 |
| Report Date: |
Jan 2011 |
| Report Number: |
A113955 |
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