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Previous work also suggests that IGF\u20101 protects ODCs from cell death and enhances remyelination in models of toxin\u2010induced and autoimmune demyelination. However, since evidence remains controversial, the therapeutic potential of IGF\u20101 in demyelinating CNS conditions is unclear. To finally shed light on the function of IGF1\u2010signaling for ODCs, we deleted insulin\u2010like growth factor 1 receptor (IGF1R) specifically in mature ODCs of the mouse. We found that ODC survival and myelin status were unaffected by the absence of IGF1R until 15\u2009months of age, indicating that IGF\u20101 signaling does not play a major role in post\u2010mitotic ODCs during homeostasis. Notably, the absence of IGF1R did neither affect ODC survival nor myelin status upon cuprizone intoxication or induction of experimental autoimmune encephalomyelitis (EAE), models for toxic and autoimmune demyelination, respectively. Surprisingly, however, the absence of IGF1R from ODCs protected against clinical neuroinflammation in the EAE model. 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