• LIN28A expression is downregulated in oligodendrocyte precursor cells (OPCs) in a mouse model of preterm white matter injury (PWMI), linking its deficiency to impaired myelinogenesis.
• Postnatal knockout of Lin28a in OPCs reduces OPC differentiation and myelin formation, leading to cognitive deficits in mice.
• Overexpression of LIN28A in OPCs promotes OPC differentiation and enhances myelinogenesis, rescuing cognitive impairments in PWMI mice.
• The study identifies LIN28A as a critical regulator of postnatal myelinogenesis and a potential therapeutic target for treating PWMI.