Department of Chemistry, Center for Misfolding Diseases, University of Cambridge, Cambridge, UK.
Laboratory of Organic Chemistry & Laboratory of Physical Chemistry, Wageningen University, Wageningen, The Netherlands.
Nat Commun. 2021 Jan 29;12(1):688. doi: 10.1038/s41467-020-20782-0.
Significant efforts have been devoted in the last twenty years to developing compounds that can interfere with the aggregation pathways of proteins related to misfolding disorders, including Alzheimer's and Parkinson's diseases. However, no disease-modifying drug has become available for clinical use to date for these conditions. One of the main reasons for this failure is the incomplete knowledge of the molecular mechanisms underlying the process by which small molecules interact with protein aggregates and interfere with their aggregation pathways. Here, we leverage the single molecule morphological and chemical sensitivity of infrared nanospectroscopy to provide the first direct measurement of the structure and interaction between single Aβ42 oligomeric and fibrillar species and an aggregation inhibitor, bexarotene, which is able to prevent Aβ42 aggregation in vitro and reverses its neurotoxicity in cell and animal models of Alzheimer's disease. Our results demonstrate that the carboxyl group of this compound interacts with Aβ42 aggregates through a single hydrogen bond. These results establish infrared nanospectroscopy as a powerful tool in structure-based drug discovery for protein misfolding diseases.
在过去的二十年中,人们投入了大量精力来开发可以干扰与错误折叠疾病(包括阿尔茨海默病和帕金森病)相关的蛋白质聚集途径的化合物。然而,迄今为止,这些疾病还没有可用于临床的治疗药物。造成这种失败的一个主要原因是对小分子与蛋白质聚集体相互作用并干扰其聚集途径的分子机制了解不完整。在这里,我们利用红外纳米光谱的单分子形态和化学敏感性,首次直接测量了单 Aβ42 低聚体和纤维状物种与聚集抑制剂倍他罗汀之间的结构和相互作用,该抑制剂能够在体外阻止 Aβ42 聚集并逆转其在阿尔茨海默病的细胞和动物模型中的神经毒性。我们的结果表明,该化合物的羧基基团通过单个氢键与 Aβ42 聚集体相互作用。这些结果确立了红外纳米光谱作为基于结构的蛋白质错误折叠疾病药物发现的有力工具。