After finishing my PhD program, I moved to Tohoku University in Sendai, Japan, to investigate the potential benefits of an inhibitor of plasminogen activator inhibitor 1 (PAI-1 inhibitor) for therapy of multiple sclerosis (MS). The available treatment for MS has been expanding continuously in recent years, although more efforts are needed for the development of new drugs in order to improve the efficacy of new disease-modifying agents. The goal was to characterize the role and potential benefits of PAI-1 inhibitor in MS from an interdisciplinary point of view. Using a mouse model of MS (experimental allergic encephalomyelitis), our group demonstrated that this compound protects against inflammation, ameliorates demyelination and axonal degeneration, representing a novel therapeutic approach for MS. After this, I moved to the Kentucky Spinal Cord Injury Research Center at the University of Louisville. The focus was to understand the mechanisms of axonal degeneration after spinal cord injury (SCI). We showed a differential expression of the ryanodine receptor isoforms following SCI using an intravital two-photon microscope in vivo. This finding could explain the role of this intra-axonal calcium channel during secondary damage after injury. Currently at the Medical College of Wisconsin, Dr. Antje Kroner and I are investigating the role and regulation of specific cytokines and chemokines such as CCL3 during secondary damage after SCI in a contusion mice model. The aim is to understand alternatives to modulating the activated immune response, which ultimately is intended to protect the tissue from further damage and facilitate a better functional recovery.