Abnormal interaction of amyloid-β peptide (Aβ) and metal ions is proved to be related to the etiology of Alzheimer's disease (AD). Using metal chelators to reverse metal-triggered Aβ aggregation has become one of the potential therapies for AD. In our work, the effect of metal chelator, NBD-BPEA, on Zn²⁺- or Cu²⁺-mediated Aβ₄₀ aggregation and neurotoxicity has been systematically studied. NBD-BPEA exhibits the capability to inhibit the metal-mediated Aβ₄₀ aggregation and disassemble performed Aβ₄₀ aggregates. It also prevents the formation of the β-sheet structure and promotes the reversion of the β-sheet to the normal random coil conformation. Moreover, it can alleviate Zn²⁺- or Cu²⁺-Aβ₄₀-induced neurotoxicity, suppress the intracellular ROS and protect against cell apoptosis. These preliminary findings indicate that NBD-BPEA has promising perspective of application in the treatment of AD, and therefore deserve further investigation as potential anti-AD agents.

淀粉样蛋白-β肽（Aβ）和金属离子的异常相互作用被证明与阿尔茨海默氏病（AD）的病因有关。使用金属螯合剂逆转金属触发的Aβ聚集已成为AD的潜在疗法之一。在我们的工作中，已经系统地研究了金属螯合剂NBD-BPEA对Zn ²⁺或Cu ²⁺介导的_Aβ40聚集和神经毒性的影响。NBD-BPEA表现出抑制金属介导的_Aβ40聚集和分解进行的_Aβ40聚集体的能力。它还防止了β-折叠结构的形成，并促进了β-折叠恢复为正常的无规卷曲构象。此外，它可以减轻Zn 2 ⁺ -或Cu²⁺ -Aβ ₄₀诱导的神经毒性，抑制细胞内ROS并防止细胞凋亡。这些初步发现表明，NBD-BPEA在治疗AD中具有广阔的应用前景，因此作为潜在的抗AD药物值得进一步研究。