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Amyloid β-protein oligomers and Alzheimer’s disease

机译：淀粉样β蛋白寡聚体和阿尔茨海默氏病

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The oligomer cascade hypothesis, which states that oligomers are the initiating pathologic agents in Alzheimer’s disease, has all but supplanted the amyloid cascade hypothesis, which suggested that fibers were the key etiologic agents in Alzheimer’s disease. We review here the results of in vivo , in vitro and in silico studies of amyloid β-protein oligomers, and discuss important caveats that should be considered in the evaluation of these results. This article is divided into four sections that mirror the main approaches used in the field to better understand oligomers: (1) attempts to locate and examine oligomers in vivo in situ ; that is, without removing these species from their environment; (2) studies involving oligomers extracted from human or animal tissues and the subsequent characterization of their properties ex vivo ; (3) studies of oligomers that have been produced synthetically and studied using a reductionist approach in relatively simple in vitro biophysical systems; and (4) computational studies of oligomers in silico . These multiple orthogonal approaches have revealed much about the molecular and cell biology of amyloid β-protein. However, as informative as these approaches have been, the amyloid β-protein oligomer system remains enigmatic.
机译：寡聚体级联假说声称寡聚体是阿尔茨海默氏病的始发性病原体，几乎取代了淀粉样蛋白级联假说，这表明纤维是阿尔茨海默氏病的关键病原体。我们在这里回顾了淀粉样β蛋白寡聚体的体内，体外和计算机模拟研究结果，并讨论了在评估这些结果时应考虑的重要警告。本文分为四个部分，它们反映了本领域中用来更好地理解寡聚物的主要方法：（1）尝试在体内原位定位和检查寡聚物;也就是说，不将这些物种从其环境中移出; （2）研究涉及从人或动物组织中提取的低聚物及其在体外的特性表征; （3）在比较简单的体外生物物理系统中合成的寡聚物的研究，并采用还原论方法进行研究; （4）计算机中低聚物的计算研究。这些多种正交方法揭示了许多有关淀粉样β蛋白的分子和细胞生物学的知识。然而，尽管这些方法提供了很多信息，但淀粉样蛋白β-蛋白寡聚体系统仍然是一个谜。

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