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Semmes Foundation, Distinguished Chair in Neurobiology College of Sciences, The University of Texas at San Antonio, USA
His studies are focused on the mechanism of formation and physiological consequences of the cytopathology of Alzheimer disease. We have shown that oxidative damage is the initial cytopathology in Alzheimer disease. They are working to determine the sequence of events leading to neuronal oxidative damage and the source of the increased oxygen radicals. Their current studies focus on (i) the mechanism for RNA-based redox metal binding; (ii) the consequences of RNA oxidation on protein synthesis rate and fidelity; (iii) the role of redox active metals in mediating prooxidant and antioxidant properties; (iv) the signal transduction pathways altered in Alzheimer disease that allow neurons to evade apoptosis; and (v) mechanism of phosphorylation control of oxidative damage to neurofilament proteins.