Characterization of the Rac1 effector moleculaes which trigger neuronal death induced by Aß peptide. Role of oxidative stressand PYG in this process.
Examination of whether Aß peptide signals to PYG through Rac1 and leads to glycogenolysis in neurons.
The knowledge generated from the previous objectives will be useful to tacked in vitro therapeutic strategies that will allow using organic molecules or permeable peptides to block at molecular level the death program induced by the Aß peptide.
