School of Chemistry, Dalian University of Technology, Dalian, China.
J Comput Aided Mol Des. 2012 Aug;26(8):963-76. doi: 10.1007/s10822-012-9588-4. Epub 2012 Jul 25.
The pathogenesis of Alzheimer's disease (AD) has been suggested to be related with the aggregation of amyloid β (Aβ) peptides. Metal ions (e.g. Cu, Fe, and Zn) are supposed to induce the aggregation of Aβ. Recent development of bifunctional molecules that are capable of interacting with Aβ and chelating biometal ions provides promising therapeutics to AD. However, the molecular mechanism for how Aβ, metal ions, and bifunctional molecules interact with each other is still elusive. In this study, the binding mode of Zn(2+)-bound Aβ with bifunctional molecules was investigated by the combination of conformational sampling of full-length Aβ peptides using replica exchange molecular dynamics simulations (REMD) and conformational selection using molecular docking and classical MD simulations. We demonstrate that Zn(2+)-bound Aβ((1-40)) and Aβ((1-42)) exhibit different conformational ensemble. Both Aβ peptides can adopt various conformations to recognize typical bifunctional molecules with different binding affinities. The bifunctional molecules exhibit their dual functions by first preferentially interfering with hydrophobic residues 17-21 and/or 30-35 of Zn(2+)-bound Aβ. Additional interactions with residues surrounding Zn(2+) could possibly disrupt interactions between Zn(2+) and Aβ, which then facilitate these small molecules to chelate Zn(2+). The binding free energy calculations further demonstrate that the association of Aβ with bifunctional molecules is driven by enthalpy. Our results provide a feasible approach to understand the recognition mechanism of disordered proteins with small molecules, which could be helpful to the design of novel AD drugs.
阿尔茨海默病(AD)的发病机制被认为与淀粉样β(Aβ)肽的聚集有关。金属离子(例如 Cu、Fe 和 Zn)被认为会诱导 Aβ的聚集。能够与 Aβ相互作用并螯合生物金属离子的双功能分子的最新发展为 AD 提供了有希望的治疗方法。然而,Aβ、金属离子和双功能分子如何相互作用的分子机制仍不清楚。在这项研究中,通过使用 replica exchange 分子动力学模拟(REMD)对全长 Aβ肽进行构象采样和使用分子对接和经典 MD 模拟进行构象选择相结合,研究了 Zn(2+)-结合 Aβ与双功能分子的结合模式。我们证明 Zn(2+)-结合的 Aβ((1-40))和 Aβ((1-42))表现出不同的构象整体。这两种 Aβ肽都可以采用各种构象来识别具有不同结合亲和力的典型双功能分子。双功能分子通过首先优先干扰 Zn(2+)-结合的 Aβ的疏水性残基 17-21 和/或 30-35 来发挥其双重功能。与 Zn(2+)周围残基的额外相互作用可能会破坏 Zn(2+)与 Aβ之间的相互作用,从而促进这些小分子螯合 Zn(2+)。结合自由能计算进一步证明,Aβ与双功能分子的结合是由焓驱动的。我们的研究结果提供了一种理解无序蛋白与小分子相互作用的识别机制的可行方法,这可能有助于设计新型 AD 药物。