Impaired oligodendrocyte maturation in preterm XXXX : Potential therapeutic targets.

@entity1545 @entity1 @entity32 @entity132 @entity73 @entity71 @entity26 @entity72 @entity62
Preterm birth is an evolving challenge in neonatal health care. Despite declining mortality rates among extremely premature neonates, morbidity rates remain very high. Currently, perinatal diffuse @entity62 ( @entity62 ) is the most commonly observed type of @entity1545 in preterm @entity1 and has become an important research area. Diffuse @entity62 is associated with @entity73 and is increasingly being recognized as a risk factor for @entity72 , @entity71 , and other @entity132 . No treatment options are currently available for diffuse @entity62 and the underlying pathophysiological mechanisms are far from being completely understood. Preterm birth is associated with maternal @entity32 , perinatal infections and disrupted @entity26 supply which can affect the cerebral microenvironment by causing activation of microglia, astrogliosis, excitotoxicity, and oxidative stress. This intricate interplay of events negatively influences oligodendrocyte development, causing arrested oligodendrocyte maturation or oligodendrocyte cell death, which ultimately results in myelination failure in the developing white matter. This review discusses the current state in perinatal @entity62 research, ranging from a clinical perspective to basic molecular pathophysiology. The complex regulation of oligodendrocyte development in healthy and pathological conditions is described, with a specific focus on signaling cascades that may play a role in @entity62 . Furthermore, emerging concepts in the field of @entity62 and issues regarding currently available animal models are put forward. Novel insights into the molecular mechanisms underlying impeded oligodendrocyte maturation in diffuse @entity62 may aid the development of novel treatment options which are desperately needed to improve the quality-of-life of preterm neonates.
