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Inflammatory signature of cerebellar neurodegeneration during neonatal hyperbilirubinemia in Ugt1-/- mouse model

机译:Ugt1-/-小鼠模型中新生儿高胆红素血症期间小脑神经退行性炎的炎症信号

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摘要

BackgroundSevere hyperbilirubinemia is toxic during central nervous system development. Prolonged and uncontrolled high levels of unconjugated bilirubin lead to bilirubin-induced neurological damage and eventually death by kernicterus. Bilirubin neurotoxicity is characterized by a wide array of neurological deficits, including irreversible abnormalities in motor, sensitive and cognitive functions, due to bilirubin accumulation in the brain. Despite the abundant literature documenting the in vitro and in vivo toxic effects of bilirubin, it is unclear which molecular and cellular events actually characterize bilirubin-induced neurodegeneration in vivo.
机译:背景严重的高胆红素血症在中枢神经系统发育过程中具有毒性。长时间且不受控制的高水平未结合胆红素会导致胆红素引起的神经系统损害,并最终因角膜白斑而死亡。胆红素的神经毒性的特征是由于脑中胆红素的积聚而导致多种神经功能缺损,包括运动,敏感和认知功能的不可逆异常。尽管有大量文献记录了胆红素在体外和体内的毒性作用,但尚不清楚哪些分子和细胞事件实际上是体内胆红素诱导的神经变性的特征。

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