Recent results indicated that exogenous D-aspartate (D-Asp) administration might represent a novel treatment strategy for stimulating myelin recovery after demyelination. D-Asp possesses neuroprotective properties to prevent/delay the onset of the experimental autoimmune encephalomyelitis (EAE) and to attenuate the severity of the disease. D-Asp treatment reduced inflammation and decreased the level of interleukin 6 in the serum compared to control animals, coupled to higher antioxidant capacity. Intra-peritoneal administration of D-Asp in EAE mice resulted in lower demyelination, leukocyte margination, perivascular cuffing, and hypercellularity in the cerebellum (Goudarzvand et al., 2019). Treatment with D-Asp on oligodendrocyte lineage cells in the cuprizone model, during both demyelination and remyelination, significantly enhanced motor coordination and balance, avoided oligodendrocytes and myelin loss and affected the upregulation of astrocyte and microglial inflammatory markers in the corpus callosum during demyelination (de Rosa et al., 2019). D-Asp treatment also stimulated axonal myelination during developmental myelination in organotypic cerebellar slices.