Disturbed iron metabolism in phagocytes as a driver of chronic inflammation – a model of MS progression?

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:

    1. What role plays the Fth1 expression in phagocytes for the resolution of demyelinating lesions?
    2. What functions does Fth1 have in demyelinating lesions?
    3. Does iron chelation have the potential to prevent chronic inflammation and progressive neurodegeneration?

Dynamic tracking of Fth1 expresssion in phagocytes

 

 

 

 

 

 

 

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

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