Die Rolle der Rezeptor-Protein-Tyrosin-Phosphatase Typ ζ bei der De- und Remyelinisierung

Abstract

Multiple Sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by disruption of the blood-brain barrier, inflammation, demyelination, loss of oligodendrocytes, axonal damage and reactive gliosis. The extent of remyelination is highly variable between patients. The receptor protein tyrosine phosphatase type ζ (RPTPζ) is primarily expressed by oligodendrocytes, astrocytes and neurons in the CNS. Previous work has shown that RPTPζ seems to be important for myelin formation and remyelination in the context of recovery from experimental demyelinating diseases. This work examines the effects of RPTPζ deficiency in the cuprizone mouse model of toxic demyelination focusing on the extent of de- and remyelination, the loss of mature oligodendrocytes, the recruitment/differentiation of oligodendrocyte precursor cells, axonal damage and infiltration of CD3+-T-cells and activated microglia into the mouse corpus callosum. For this purpose demyelination was induced in wildtype and RPTPζ-deficient mice. We did not observe significant differences regarding the extent of de- and remyelination or the cellular processes listed above. In summary, the lack of RPTPζ does not influence the extent of de- and remyelination, the loss of mature oligodendrocytes, recruitment/differentiation of oligodendrocyte precursor cells, axonal damage or infiltration of CD3+-T-cells and activated microglia in the cuprizone model.