【摘要】 β-淀粉样肽(amyloid-βpeptide,Aβ)是阿尔采末病患者脑内老年斑的主要成分,具有很强的神经毒性。近年来,研究发现细胞内产生和聚集的Aβ可以通过多种途径发挥其神经毒性作用。利用离体线粒体模型发现,Aβ可以导致线粒体通透性转变孔道(mitochondrial permeability transition pore,MPTP)开放。MPTP开放会进一步加剧线粒体功能的损伤,并可导致细胞色素c和凋亡诱导因子释放,在线粒体介导的细胞死亡中具有重要作用。Aβ引起的MPTP开放可能是胞内Aβ导致神经元死亡的重要通路,研究Aβ对该孔道的影响将有助于阐明Aβ的毒性机理并以期找到减轻Aβ损伤的新策略。更多还原

【Abstract】 Amyloid-β(Aβ),the main constituent of senile plaques in the brain of Alzheimer’s disease (AD) patients,has been demonstrated to be neurotoxic both in vivo and in vitro.Recently,intracellular Aβhas been widely found to exert its neurotoxicity through multiple pathways.Accumulating studies,based on the isolated mitochondria,have reported that Aβcould induce the opening of mitochondrial permeability transition pore (MPTP),aggravate mitochondrial dysfunction,and eventually result in the release of cytochrome c and apoptosis- inducing-factor from mitochondria,which may underlie the mechanisms of intracellular Aβinduced neurotoxicity. Efforts on elucidating MPTP involvement in Aβaction are anticipated to be helpful to find new ways attenuating Aβ-induced neurotoxicity.更多还原