Figure 1.

Preclinical models of encephalopathy of prematurity (EoP) include preterm deliveries in non-human primates, and in other mammals chorioamnionitis induced by intra-amniotic or intrauterine endotoxin and/or hypoxia-ischemia mimicking placental underperfusion. These primary approaches to recapitulating CNS injury associated with preterm birth lead to loss of oligodendroglial lineage cells and axonal injury, premature subplate loss, loss of thalamic neurons, and loss of migrating GABAergic neurons, the key components of EoP. Cumulatively, the cellular and molecular abnormalities manifest as imaging abnormalities, motor deficits, propensity to seizures, and impaired cognition and behavior in the mature brain. EoP leads to cerebral palsy, epilepsy, cognitive deficits, and behavioral abnormalities such as anxiety, attention-deficit disorder and autism.