Epilepsy is a neurological disorder characterized by epileptic seizures, but pathology and progression differs widely among epilepsy cases. Seizures are the results of abnormal and excessive brain activity, and lead to brain injury and contribute to neuronal death. Evidence from clinical and experimental studies indicates that brain inflammation is an intrinsic feature of the hyperexcitable pathologic brain tissue in epilepsy.5 Oxidative stress is known to be implicated in the initiation and progression of the diseases. It is suspected that epileptic seizures are a consequence of an imbalance of oxidant-antioxidants compounds. There are increasing evidence of the involvement of inflammatory mediators, and it’s known that seizure leads to inflammation at the same time that inflammation enhances predisposition to seizures. In this context, CeO₂NPs have been extensively studied due to their tissue protective properties, degrading toxic excess of free radicals. CeO₂NPs have high capacity to buffer electrons in redox environments, followed by the capture or release of oxygen. This means that CeO2NPs act as a freeradical scavenger of ROS molecules such as OH• and H₂O₂.

Production of CeO₂ library with neuropharmaceuticals and neurotransporters.

Evaluation of the best in vitro translocation compound in the blood brain barrier.

Evaluation of brain penetration of the best compound in vivo

Therapeutic evaluation in brain of the best compound in vivo