B13
Over the course of multiple sclerosis there are different ways how MS lesions can evolve. While some lesions can resolve, persistent phagocyte activation is observed in chronic-active lesions. Currently, we do not understand which factors determine the fate of MS lesions. Here, we hypothesize that the balance between iron release and buffering is a key switch that determines whether an inflammatory CNS lesion will resolve or persists. In the proposed project we therefore plan to char-acterize the regulation of iron buffering in demyelinating lesions, define its importance for lesion fate and explore its potential as a therapeutic target. Our research questions are:
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- What role plays the Fth1 expression in phagocytes for the resolution of demyelinating lesions?
- What functions does Fth1 have in demyelinating lesions?
- Does iron chelation have the potential to prevent chronic inflammation and progressive neurodegeneration?
Principal Investigators:
Univ.-Prof. Dr. med. Mikael Simons
Institut für Neuronale Zellbiologie
TU München
msimons@gwdg.de
Univ.-Prof. Dr. med. Martin Kerschensteiner
Institut für Klinische Neuroimmunologie
München
martin.kerschensteiner@med.uni-muenchen.de