Although the survival rates of preterm infants have markedly improved, their neurodevelopmental outcomes remain poor. Historically, brain injury in preterm infants has been recognized as intraventricular hemorrhage or white matter injury, often resulting in cerebral palsy. More recently, increasing attention has focused on the elevated risk of neurodevelopmental disorders among preterm infants across a wide range of gestational ages. Furthermore, preterm birth is also associated with an increased risk of psychiatric disorders in adulthood, including depression and schizophrenia. However, the underlying pathophysiology of these conditions remains poorly understood, and therapeutic strategies and their efficacy are limited. Preterm birth occurs during a critical period of brain development, when processes including neurogenesis, gliogenesis, and oligodendrocyte maturation are actively progressing. In addition, recent studies have demonstrated that in humans, neural stem cells (NSCs) persist in the ventricular-subventricular zone (V-SVZ) during the early postnatal period and continue to generate new neurons. Early postnatal neurogenesis may therefore contribute to brain development during infancy. Although preterm birth may disrupt these developmental processes, its impact on brain development during this critical period remains incompletely understood. We recently discovered that preterm birth causes decreased early postnatal neurogenesis in the V-SVZ in both mice and humans, and proposed this as a novel mechanism underlying adverse neurodevelopmental outcomes in preterm infants. These findings indicate that targeting postnatal NSC function may provide a new therapeutic approach for neurodevelopmental disorders in preterm infants. Our findings also provide new insights into the mechanisms underlying various long-term complications of preterm birth.