Department of Biochemistry, Virginia Polytechnic Institute & State University, Blacksburg, VA 24061, USA.
Department of Biochemistry, Virginia Polytechnic Institute & State University, Blacksburg, VA 24061, USA; BRITE Research Institute and Department of Pharmaceutical Sciences, North Carolina Central University, Durham, NC 27707, USA; Affiliated Faculty, Duke/UNC Alzheimer's Disease Research Center, Durham, NC 27710, USA.
Pharmacol Res. 2022 Oct;184:106409. doi: 10.1016/j.phrs.2022.106409. Epub 2022 Aug 20.
A range of neurodegenerative and related aging diseases, such as Alzheimer's disease and type 2 diabetes, are linked to toxic protein aggregation. Yet the mechanisms of protein aggregation inhibition by small molecule inhibitors remain poorly understood, in part because most protein targets of aggregation assembly are partially unfolded or intrinsically disordered, which hinders detailed structural characterization of protein-inhibitor complexes and structural-based inhibitor design. Herein we employed a parallel small molecule library-screening approach to identify inhibitors against three prototype amyloidogenic proteins in neurodegeneration and related proteinopathies: amylin, Aβ and tau. One remarkable class of inhibitors identified from these screens against different amyloidogenic proteins was catechol-containing compounds and redox-related quinones/anthraquinones. Secondary assays validated most of the identified inhibitors. In vivo efficacy evaluation of a selected catechol-containing compound, rosmarinic acid, demonstrated its strong mitigating effects of amylin amyloid deposition and related diabetic pathology in transgenic HIP rats. Further systematic investigation of selected class of inhibitors under aerobic and anaerobic conditions revealed that the redox state of the broad class of catechol-containing compounds is a key determinant of the amyloid inhibitor activities. The molecular insights we gained not only explain why a large number of catechol-containing polyphenolic natural compounds, often enriched in healthy diet, have anti-neurodegeneration and anti-aging activities, but also could guide the rational design of therapeutic or nutraceutical strategies to target a broad range of neurodegenerative and related aging diseases.
一系列神经退行性疾病和相关衰老疾病,如阿尔茨海默病和 2 型糖尿病,与毒性蛋白聚集有关。然而,小分子抑制剂抑制蛋白聚集的机制仍知之甚少,部分原因是大多数聚集组装的蛋白靶标部分展开或固有无序,这阻碍了对蛋白-抑制剂复合物的详细结构表征和基于结构的抑制剂设计。在此,我们采用平行小分子文库筛选方法来鉴定针对神经退行性变和相关蛋白病中的三种原型淀粉样蛋白原蛋白的抑制剂:胰岛淀粉样多肽、Aβ 和 tau。从这些针对不同淀粉样蛋白原蛋白的筛选中鉴定出的一类显著的抑制剂是含有儿茶酚的化合物和与氧化还原相关的醌/蒽醌。对鉴定出的大多数抑制剂进行了二次测定验证。对所选儿茶酚类化合物之一迷迭香酸的体内功效评估表明,其对 HIP 转基因大鼠的胰岛淀粉样多肽沉积和相关糖尿病病理学具有很强的缓解作用。在有氧和无氧条件下对选定类抑制剂的进一步系统研究表明,含有儿茶酚的广泛化合物类的氧化还原状态是淀粉样蛋白抑制剂活性的关键决定因素。我们获得的分子见解不仅解释了为什么许多含有儿茶酚的多酚类天然化合物,通常富含于健康饮食中,具有抗神经退行性和抗衰老活性,而且还可以指导针对广泛神经退行性疾病和相关衰老疾病的治疗或营养策略的合理设计。