Mal'tsev A V, Galzitskaia O V
Biomed Khim. 2010 Nov-Dec;56(6):624-38.
Studies of neurodegenetrative disorders have become particularly actual attracting the attention of researchers from over the world because of the dissemination of Alzheimer's disease. The reason for such pathogenesis is the transition of a "healthy" molecule or peptide from the native conformation into a very stable "pathological" isoform. During this, molecules in the "pathological" conformation aggregate, forming amyloid fibrils that can increase without any control. Novel knowledge is required on sporadic isoforms of Alzheimer's disease, on the nature of triggering mechanisms of conformational transitions of beta-amyloid fragments from normally functioning proteins into new formations--nano-beta-amyloids--that spiral out of control of neurons and organism which leads to the loss of neurons. Herein we review studies devoted to the formation of amyloid fibrils and their role in pathogenesis of amyloid diseases.
由于阿尔茨海默病的传播,神经退行性疾病的研究变得尤为迫切,吸引了来自世界各地的研究人员的关注。这种发病机制的原因是“健康”分子或肽从天然构象转变为非常稳定的“病理”异构体。在此过程中,处于“病理”构象的分子聚集,形成淀粉样原纤维,且其会不受控制地增加。对于阿尔茨海默病的散发性异构体,以及β-淀粉样片段从正常功能蛋白转变为新形成物——纳米β-淀粉样蛋白——的构象转变触发机制的本质,我们需要新的认识,这种新形成物会脱离神经元和机体的控制,导致神经元丧失。在此,我们综述了关于淀粉样原纤维形成及其在淀粉样疾病发病机制中作用的研究。