Abstract
Abstract—According to modern ideas, the basis of intellectual problems in neurological brain damage is active forgetting, regulated by Rac and Rho small GTPases-dependent signal stages of actin remodeling. The key enzyme of these cascades is LIM kinase 1 (LIMK1). Changes in limk1 gene expression lead to neurocognitive pathologies. Rapid screening and testing of targeted therapeutic agents modifying protein-protein interactions of GTPases and components of signaling cascades requires the development and validation of simple animal models. Such an opportunity is provided by Drosophila, the mutant strains of which allow you to identify the nodal moments of intersection of biochemical and neural networks, accompanying active forgetting.
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