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Repair of myelin injury in multiple sclerosis may fail, resulting in chronic demyelination, axonal loss, and disease progression. As cellular pathways regulated by phosphatase and tensin homologue deleted on chromosome 10 (PTEN; eg, phosphatidylinositol‐3‐kinase [PI‐3K]) have been reported to enhance axon regeneration and oligodendrocyte maturation, we investigated potentially beneficial effects of Pten loss of function in the oligodendrocyte lineage on remyelination.

We characterized oligodendrocyte numbers and myelin sheath thickness in mice with conditional inactivation of Pten in oligodendrocytes, Olig2‐cre, Pten^fl/fl mice. Using a model of central nervous system demyelination, lysolecithin injection into the spinal cord white matter, we performed short‐ and long‐term lesioning experiments and quantified oligodendrocyte maturation and myelin sheath thickness in remyelinating …