Dr. Rieger is interested in mechanisms leading to peripheral neuropathy, such as induced by chemotherapy or diabetes. Her research uncovered a potential target in the treatment of these conditions. Her lab showed that the chemotherapeutic agent, paclitaxel, and high glucose levels in a model of diabetic neuropathy, increase the formation of H2O2 in epidermal keratinocytes. Elevated H2O2 levels activate the matrix-degrading metalloproteinase, MMP-13, which induces cell adhesion defects and degeneration of unmyelinated sensory axons. Her work further showed that pharmacological inhibition of MMP-13 prevents paclitaxel and glucose neurotoxicity in rodent models, providing evidence that the mechanism may potentially be conserved in humans. Her current research is focused on identifying how paclitaxel induces the production H2O2 and what precise role MMP-13 plays in axon degeneration. Her goal is to work toward the development of neuropathy treatments.