Institute of Biochemical Sciences, National Taiwan University, Taipei, Taiwan; Genomics Research Center, Academia Sinica, Taipei, Taiwan.
Small. 2012 Dec 7;8(23):3631-9. doi: 10.1002/smll.201201068. Epub 2012 Aug 23.
Amyloids are pathogenic hallmarks in many neurodegenerative diseases such as amyloid-β (Aβ) fibrils in Alzheimer's disease (AD). Here, the effect of gold nanoparticles (AuNPs) on amyloids is examined using Aβ as a model system. It is found that bare AuNPs inhibited Aβ fibrillization to form fragmented fibrils and spherical oligomers. Adding bare AuNPs to preformed Aβ fibrils results in ragged species where AuNPs bind preferentially to fibrils. Similar results are demonstrated with carboxyl- but not amine-conjugated AuNPs. Co-incubation of negatively charged AuNPs with Aβ relieved Aβ toxicity to neuroblastoma. Overall, it is demonstrated that AuNPs possessing negative surface potential serve as nano-chaperones to inhibit and redirect Aβ fibrillization, which could contribute to applications for AD.
淀粉样蛋白是许多神经退行性疾病的致病特征，如阿尔茨海默病（AD）中的淀粉样β（Aβ）纤维。在这里，使用 Aβ 作为模型系统来检查金纳米粒子（AuNPs）对淀粉样蛋白的影响。结果发现，裸露的 AuNPs 抑制了 Aβ 的纤维化，形成了碎片化的纤维和球形低聚物。将裸露的 AuNPs 添加到预先形成的 Aβ 纤维中会导致纤维变得参差不齐，AuNPs 优先与纤维结合。羧基修饰的 AuNPs 而不是氨基修饰的 AuNPs 表现出类似的结果。带负电荷的 AuNPs 与 Aβ 共孵育可减轻 Aβ 对神经母细胞瘤的毒性。总的来说，结果表明具有负表面电势的 AuNPs 可作为纳米伴侣抑制和重定向 Aβ 纤维化，这可能有助于 AD 的应用。
