- Anti-oxidant/anti-inflamatory nanoparticles to protect the brain from excess electrophysiology and to mitigate damage post-crisis
- Characterization of the didys552 zebrafish mutant line (mutation in snc1lab gene) and set up of an efficacy drug screening assay using reference compounds
- Cell Therapy with GABAergic interneuron precursors for Early Infantil Epileptic Encephalopathies (S. Dravet, S. West y S. Stxbp1)
- Creation of a therapeutic drug monitoring (TDM) unit for the optimization of the Dravet syndrome pharmacological therapy
- Design, synthesis and pharmacological evaluation of new neuroprotective agents oriented to the tratment of Dravet syndrome
- Efecto de campos magnéticos estáticos de intensidad moderada en modelos de epilepsia y síndrome de Dravet
- The effect of beta-caryophyllene treatment in a murine model of Dravet syndrome
- The endocannabinoid system study in Dravet syndrome
- Intrinsic neuronal excitability and spontaneous 1 activity underlie cortical abnormalities upon Nr2f1/COUP-TFI deficiency
- Investigating Epilepsy by Super-resolution Imaging of Synapses and the Extracellular Space in Live Brain Tissue
- Precision Medicine in Dravet Syndrome
- Reactive Neurogenesis and Gliogenesis in a Dravet Syndrome Mouse Model
Timeline: First phase (design of conjugates and verification of their ability to reach the brain and its therapeutic effect in murine models): 150,000 euros.
Project: Anti-oxidant/anti-inflamatory nanoparticles to protect the brain from excess electrophysiology and to mitigate damage post-crisis.
Scientific groups: In collaboration with Dr. Juanma Encinas (Basque Center for Neuroscience Achucarro ), Ibo Galindo (Principe Felipe Ivestigation center)
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