Our Research Focus
Abnormal excitability contributes to neurologic disease pathogenesis either by impairing cell function or by increasing cellular susceptibility to injury. In most neurologic diseases, the pathologic process does not involve the entire brain-muscle functional unit. Instead, only specific subsets of neurons, glial cells, or muscle fibers are injured or die, and the nature of this selective injury determines the symptoms and clinical course of each disease. The long-term goal of our laboratory is to elucidate how ion channel signaling and synaptic plasticity contribute to the selective vulnerability of different cell populations and thus influence onset and/or progression of different neurologic disorders. We use a combination of different approaches (molecular and cell biology, immunohistochemistry, imaging, biochemistry, and electrophysiology) to investigate two distinct but related areas: (1) the function of intrinsic antioxidant signaling in the brain and skeletal muscle and (2) the role of autophagy impairment in neurologic disease pathogenesis.