Oligodendrocyte Development and Implication in Perinatal White Matter Injury

Perinatal white matter injury (WMI) is the most common brain injury in premature infants and can lead to life-long neurological deficits such as cerebral palsy. Preterm birth is typically accompanied by inflammation and hypoxic-ischemic events. Such perinatal insults negatively impact maturation of oligodendrocytes (OLs) and cause myelination failure. At present, no treatment options are clinically available to prevent or cure WMI. Given that arrested OL maturation plays a central role in the etiology of perinatal WMI, an increased interest has emerged regarding the functional restoration of these cells as potential therapeutic strategy. Cell transplantation and promoting endogenous oligodendrocyte function are two potential options to address this major unmet need. In this review, we highlight the underlying pathophysiology of WMI with a specific focus on OL biology and their implication for the development of new therapeutic targets.

Automated summary

Perinatal white matter injury is common in premature infants and can lead to lifelong neurological deficits. The immaturity of oligodendrocytes and failure of myelination are the key factors in the etiology of this condition. Currently, there are no clinical treatment options available, leading to increased interest in cell transplantation and promoting endogenous oligodendrocyte function as potential therapeutic strategies.