Choudhury Arunabh, Khan Sumaiya, Saeed Mohammad Umar, Mohammad Taj, Hussain Afzal, AlAjmi Mohamed F, Fatima Urooj, Islam Asimul, Hassan Md Imtaiyaz
Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, Jamia Nagar, New Delhi, 110025, India.
Department of Pharmacognosy, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Biochem Biophys Res Commun. 2025 Aug 15;775:152166. doi: 10.1016/j.bbrc.2025.152166. Epub 2025 Jun 8.
Tauopathies are a class of nearly 20 neurodegenerative diseases, classified into primary and secondary tauopathies. Alzheimer's disease (AD) is a type of secondary tauopathy in which abnormal phosphorylation of tau proteins takes place, which is linked to the kinase activity of dual-specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A). Overexpression of DYRK1A hyperphosphorylates the tau protein, leading to its aggregation. Inhibiting DYRK1A activity can be a promising strategy to prevent tau hyperphosphorylation. In this study, we conducted a virtual screening of natural bioactive compounds from the ZINC database to identify potential small-molecule inhibitors of DYRK1A. The analyses revealed two compounds, ZINC08300244 and ZINC08964763, which showed a high binding affinity with DYRK1A and appropriate pharmacokinetic properties. Density functional theory (DFT) analysis of these two compounds was performed, and their stability of interaction with DYRK1A was further analysed by all-atom molecular dynamics (MD) simulations for 1 μs. Analysis of the MD trajectories was also performed using MM/PBSA and per-residue binding free energy decomposition. The results indicated the stable complex formation of DYRK1A with the two selected molecules for DYRK1A inhibition to prevent tau-hyperphosphorylation. This study highlights the use of virtual screening and MD simulations in finding natural product-based inhibitors of DYRK1A, which may lead to the development of novel therapeutic strategies for treating neuroinflammatory diseases.
tau蛋白病是一类近20种神经退行性疾病,分为原发性和继发性tau蛋白病。阿尔茨海默病(AD)是一种继发性tau蛋白病,其中tau蛋白发生异常磷酸化,这与双特异性酪氨酸磷酸化调节激酶1A(DYRK1A)的激酶活性有关。DYRK1A的过表达使tau蛋白过度磷酸化,导致其聚集。抑制DYRK1A活性可能是预防tau蛋白过度磷酸化的一种有前景的策略。在本研究中,我们对ZINC数据库中的天然生物活性化合物进行了虚拟筛选,以鉴定DYRK1A的潜在小分子抑制剂。分析发现了两种化合物,ZINC08300244和ZINC08964763,它们与DYRK1A表现出高结合亲和力和合适的药代动力学性质。对这两种化合物进行了密度泛函理论(DFT)分析,并通过全原子分子动力学(MD)模拟1 μs进一步分析了它们与DYRK1A相互作用的稳定性。还使用MM/PBSA和每个残基的结合自由能分解对MD轨迹进行了分析。结果表明,DYRK1A与两种选定分子形成稳定的复合物,可抑制DYRK1A以防止tau蛋白过度磷酸化。本研究强调了虚拟筛选和MD模拟在寻找基于天然产物的DYRK1A抑制剂中的应用,这可能会导致开发治疗神经炎症性疾病的新治疗策略。