One of the most vexing problems in MS is to understand why some patients get worse or progress. Put another way, a frustrated patient will frequently ask “why do all the FDA treatments work only for relapsing-remitting disease and not for primary progressive (PPMS) or secondary progressive (SPMS) forms of MS?” In the past year we have continued our work to better understand the mechanisms of disease worsening using three distinct approaches and have added a fourth new avenue of exploration as follows:
Dr. Massimiliano Cristofanilli and his group are trying to determine if an experimental model can be created that allows for pathological analysis of the disease mechanisms pertaining to progressive tissue. They have already established in cell experiments and in mice that specific cellular products derived from PPMS and SPMS can replicate the disease phenotype and provide insights in understanding repair pathways. In pilot data they have shown that injecting this cellularmaterial derived from patients with progressive disease in a mouse brain leads to typical MS lesions remote from the site of injection in areas of the spinal cord (a site of disease predilection in progressive disease). This is an extremely exciting finding and is an original discovery. Confirmatory experiments are currently being performed and will for the first time allow an animal model based on human pathology to be investigated. In addition, this also has the potential of allowing the development of therapeutic strategies specifically directed at progressive disease.
Our newest avenue of research has resulted from the recruitment of Dr. Fozia Mir from University of Illinois, Chicago who joined Tisch MS in March 2011. Her expertise in cellular oxidative stress has led to initial studies in looking at isoprostanes and other oxidative stress biomarkers in patients with progressive disease.