Current Evidence on Cell Death in Preterm Brain Injury in Human and Preclinical Models.

摘要: Despite tremendous advances in neonatal intensive care over the past 20 years, prematurity carries a high burden of neurological morbidity lasting lifelong. The term encephalopathy (EoP) coined by Volpe 2009 encompasses all aspects now known effects on immature brain, including altered and disturbed development as well specific lesional hallmarks. Understanding way cells are damaged is crucial to design brain protective strategies, this purpose, preclinical models largely contribute improve comprehension cell death mechanisms. While neuronal has been deeply investigated characterized (hypoxic-ischemic) newborn at term, little about types occurring preterm injury. Three main different morphological observed specifically hypoxic-ischemic encephalopathy, namely, necrotic, apoptotic, autophagic death. Features three may be present same dying neuron. In injury, description sparse, loss primarily concerns oligodendrocytes and, infrequently, neurons. review, we first shortly discuss severe injury conditions that have reported involve death, periventricular leucomalacia (PVL), diffuse white matter (dWMI), intraventricular hemorrhages, potentially harmful iatrogenic linked premature birth (anesthesia caffeine therapy). Then, an overview current evidence concerning both clinical human tissue data focusing studies investigating presence allowing discriminating between involved. We conclude that, not only apoptosis but also other (such regulated necrotic autophagic) pathways need together order consider mechanisms involved pathogenesis damage.