Abstract
This Commentary is stimulated by a recent report by Hammond et al. [1] which utilized break-through molecular techniques to characterize microglia in multiple regions of developing brain. The work delineated a heretofore unrecognized complexity in microglial phenotypes that has implications for normal brain development, disease, dysmaturation and potential therapies. In particular the work has special relevance to the fundamental basis of the neurological disability in very premature infants, i.e., a combination of initial cerebral white matter injury (WMI), and especially, the subsequent dysmaturation involving both white matter and neuro-axonal structures [2, 3]. In the following I will discuss first the development of microglia in brain, their critical role in the genesis of both the white matter injury (WMI) and of the subsequent dysmaturation in premature brain, the pioneering new work of Hammond et al. re: microglial phenotypes, and the implications of the new data for targeted therapy in the premature infant.
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