Investigating the brain circuit and molecular alterations associated with the visuomotor integration function in CDKL5 zebrafish mutant

CDKL5 Deficiency Disorder (CDD) is a rare neurodevelopmental condition characterized by early-onset epileptic seizures, low muscle tone, progressive intellectual disability, and severe motor dysfunction. Currently, there are no effective therapies for CDD, and existing treatments primarily aim at improving symptoms rather than addressing the underlying causes of the disorder. Zebrafish offer unique advantages for the high-throughput preclinical evaluation of potential therapies for neurological diseases, including CDD. The main objective of this study is to characterize a stable zebrafish cdkl5 mutant in terms of their morphological and visually driven motor adaptation phenotype, as well as their molecular alterations. The overall goal is to provide a robust vertebrate model to enhance our understanding of the CDKL5 signaling pathway and the altered mechanisms involved in CDKL5 Deficiency Disorder. Ultimately, this research aims to contribute in he future to the identification of possible therapeutic targets for treating or alleviating the symptoms of CDD.