Entzündungsreaktionen bei CMT-Modellen: Mechanismen und Behandlungschancen

Previous studies from our laboratory have shown that in models for distinct forms of Charcot-Marie-Tooth neuropathy, phagocytosing macrophages mediate demyelination and perturbation of axons. One important mediator is colony-stimulating factor-1, unexpectedly expressed by endoneurial fibroblasts and essential for macrophage-mediated demyelination, Schwann cell dedifferentiation and axonopathy. Interestingly, macrophage-related inflammation is also a driving force for developing neuropathy in aging nerves. Further activities concerning the basic pathomechanisms are underway to decipher cell-cell communication within the peripheral nerves under disease conditions. As a translational approach, we developed distinct attempts to attenuate macrophage-related peripheral nerve inflammation as putative options to ameliorate disabling symptoms associated with CMT-1. These activities may pave the way for the development of treatment options for Charcot-Marie-Tooth neuropathies, but also for aging nerves.