fumaric acids directly influence gene expression of neuroprotective factors in rodent microglia dimethylfumarate dmf has been approved the for treatment of relapsingremitting multiple sclerosis the mode of action of dmf and its assumed active primary metabolite monomethylfumarate mmf is still not fully understood notably for brain resident cells therefore we investigated potential direct effects of dmf and mmf on microglia and indirect effects on oligodendrocytes primary rat microglia were differentiated into m1like m2like and m0 phenotypes and treated in vitro with dmf or mmf the gene expression of proinflammatory and antiinflammatory factors such as growth factors igf1 interleukins il10 il1 chemokines ccl3 cxcl10 as well as cytokines tgf1 tnf inos and the mannose receptor mrc1 was examined by determining their transcription level with qpcr and on the protein level by elisa and facs analysis furthermore microglia function was determined by phagocytosis assays and indirect effects on oligodendroglial proliferation and differentiation dmf treatment of m0 and m1like polarized microglia demonstrated an upregulation of gene expression for igf1 and mrc1 but not on the protein level while the phagocytic activity remained unchanged dmf and mmf treated microglia supernatants led to an enhanced proliferation of oligodendrocyte precursor cells opc these results suggest that dmf has antiinflammatory effects on microglia which may result in enhanced proliferation of opc