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Key roles of glial cells in the encephalopathy of prematurity
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International audience. Across the globe, approximately one in 10 babies are born preterm, that is, before37 weeks of a typical 40 weeks of gestation. Up to 50% of preterm born infantsdevelop brain injury, encephalopathy of prematurity (EoP), that substantially increasestheir risk for developing lifelong defects in motor skills and domains of learning, memory,emotional regulation, and cognition. We are still severely limited in our abilitiesto prevent or predict preterm birth. No longer just the “support cells,” we now clearlyunderstand that during development glia are key for building a healthy brain. Glialdysfunction is a hallmark of EoP, notably, microgliosis, astrogliosis, and oligodendrocyteinjury. Our knowledge of glial biology during development is exponentiallyexpanding but hasn't developed sufficiently for development of effective neuroregenerativetherapies. This review summarizes the current state of knowledge for theroles of glia in infants with EoP and its animal models, and a description of knownglial-cell interactions in the context of EoP, such as the roles for border-associatedmacrophages. The field of perinatal medicine is relatively small but has worked passionatelyto improve our understanding of the etiology of EoP coupled with detailedmechanistic studies of pre-clinical and human cohorts. A primary finding from thisreview is that expanding our collaborations with computational biologists, workingtogether to understand the complexity of glial subtypes, glial maturation, and theimpacts of EoP in the short and long term will be key to the design of therapies thatimprove outcomes.
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