Department of Pathology, Bio21 Molecular and Biotechnology Institute, University of Melbourne, Parkville, Victoria 3010, Australia.
Int J Biochem Cell Biol. 2011 Sep;43(9):1247-51. doi: 10.1016/j.biocel.2011.05.001. Epub 2011 May 11.
Whilst the amyloid-β (Aβ) hypothesis/centric theory continues to evolve, genetic, biochemical and pathological evidence still suggests that Aβ is central to the etiology of Alzheimer's disease (AD). In particular, Aβ-oligomers/soluble Aβ, may be an earlier determinant of Alzheimer's disease and better correlative of cognitive impairment. Whilst there are a number of Aβ-oligomeric species in existence (making therapeutic and diagnostic biomarker choice cumbersome), their existence is in equilibrium with Aβ-fibrils, the main constituent of cored plaques. Although Alzheimer's disease remains incurable, improvements to Aβ immunotherapies and strategies to target Aβ continue to evolve, with the reliance upon Aβ imaging to shed light on the outcome of therapeutics proving very useful.
虽然淀粉样蛋白-β（Aβ）假说/中心理论不断发展，但遗传、生化和病理学证据仍表明 Aβ 是阿尔茨海默病（AD）发病机制的核心。特别是，Aβ-寡聚体/可溶性 Aβ，可能是阿尔茨海默病的早期决定因素，并且与认知障碍的相关性更好。虽然存在许多 Aβ-寡聚体物种（使得治疗和诊断生物标志物的选择变得繁琐），但它们与 Aβ-原纤维（核心斑块的主要成分）处于平衡状态。虽然阿尔茨海默病仍然无法治愈，但 Aβ 免疫疗法和靶向 Aβ 的策略不断改进，依赖 Aβ 成像来揭示治疗效果也非常有用。
