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Ruben K. Dagda, Ph.D., received his doctoral training at the University of Iowa and his postdoctoral training at the University of Pittsburgh School of Medicine. He is currently investigating the molecular mechanisms that lead to mitochondrial dysfunction and oxidative stress in cell culture, tissue and animal models of Parkinson\s disease. He has authored in multiple research manuscripts and review articles in the areas of toxicology, toxinology, mitochondrial function, and neurobiology. As an Assistant Professor at the University of Nevada School of Medicine (UNSOM), he is committed to the training and education of undergraduate, graduate students and postdocs in his lab. His main research goals are to elucidate the prosurvival signaling pathways that regulate mitochondrial function, transport and turn-over in neurons and how aging and neurodegenerative diseases negatively impact these processes. The end goal is to develop novel small molecular drugs that can reverse neurodegeneration and elevate mitochondrial function in age-related neurodegenerative diseases.
Neurons rely on functionally efficient mitochondria to power critical neuronal functions. Given that impaired mitochondrial turnover and dysfunction underlie the etiology of many neurodegenerative diseases, understanding how reversible phosphorylation at the mitochondria regulates mitochondrial function and turnover will lay the basic groundwork for developing future “mitoprotective” therapies that reverse mitochondrial dysfunction and neurodegeneration. At the postsynaptic compartment, PINK1 and PKA remodel dendritic arbors in developing neurons and regulate mitochondrial transport. We are examining how these two kinases interact at the mitochondria and at the neurites to regulate mitochondrial function, dendritic morphology and survival. A second are of interest it to determine how mitochondrial turnover (mitophagy) is regulated by reversible phosphorylation mediated by phosphatases and kinases. A third project is to synthesize new reagents that can activate prosurvival signaling pathways at the mitochondrion as mitochondrial therapy for reversing mitochondrial pathology induced by neurodegenerative diseases.
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