The effect of neuroinflammation and oxidative stress on the recovery time of seizures

Epilepsy is a neurological disorder in which neuronal activity in the brain is disturbed resulting in recurrent seizures and is the second most common neurological disorder. Epilepsy has large impacts on patients as well as the healthcare system. Neuroinflammation and oxidative stress are both known to play a role in the occurrence and severity of seizures. When neuroinflammation occurs, oxidative stress occurs simultaneously. Oxidative stress has been shown to accelerate aging and reduce reproductivity in Caenorhabditis elegans. We tested effects of oxidative stress from seizures by evaluating the longevity, egg-laying, and electroshock resilience of C. elegans. Pseudomonas aeruginosa was used as an oxidative stressor in this experiment, resulting in neuroinflammation in C. elegans. When neuroinflammation occurs, three anti-inflammatory genes, pmk-1, elt-2, and skn-1 are activated in order to help reduce inflammation. We blocked the translation of the anti-inflammatory genes using RNAi, to assess oxidative stress without the C. elegans anti-inflammatory response when neuroinflammation was induced by adding P. aeruginosa into the C. elegans diet. Our study revealed that oxidative stress and neuroinflammation diminish longevity and reproductivity while also increasing recovery time after seizures in C. elegans. Further study backs up these findings, indicating that neuroinflammation and oxidative stress both worsen seizure severity. This research can help lead to future studies and may also lead to finding new therapeutics for epilepsy.