Thomas Mueggler1, Hartmut Pohl2, Dieter Riethmacher3, Christof Baltes1, Ueli Suter2, Markus Rudin1,4
1Institute for Biomedical Engineering, University and ETH Zurich, Zurich, Switzerland; 2Institute for Cell Biology, ETH Zurich, Zurich, Switzerland; 3Human Genetics Division, Southampton University School of Medicine, Southampton, UK; 4Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland
A novel mouse model of demyelination uses intrinsic triggering of oligodendrocyte cell death leading to progressive symptoms allowing to disentangle the role of apoptotic cell death from that of the immune system in Multiple Sclerosis. To evaluate the sensitivity of various MR readouts for monitoring the pathology we assessed T2, MTR and infiltration of macrophages in diseased and control mice. Whereas T2 hyper-intensities become apparent at a time-point of first clinical symptoms a MTR decrease is only present at progressed pathology stage. No infiltration of macrophages could be measured reflecting integrity of BBB and weak recruitment of blood-borne immune cells.