Institute of Fundamental and Applied Research, National Research University TIIAME, Kori Niyoziy 39, Tashkent 100000, Uzbekistan.
R&D Center, New Uzbekistan University, Mustaqillik Avenue 54, Tashkent 100007, Uzbekistan.
Int J Mol Sci. 2023 Mar 28;24(7):6312. doi: 10.3390/ijms24076312.
The self-association of amylogenic proteins to the fibril form is considered a pivotal factor in the pathogenesis of neurodegenerative diseases, including Parkinson's disease (PD). PD causes unintended or uncontrollable movements in its common symptoms. α-synuclein is the major cause of PD development and thus has been the main target of numerous studies to suppress and sequester its expression or effectively degrade it. Nonetheless, to date, there are no efficient and proven ways to prevent pathological protein aggregation. Recent investigations proposed applying an external electric field to interrupt the fibrils. This method is a non-invasive approach that has a certain benefit over others. We performed molecular dynamics (MD) simulations by applying an electric field on highly toxic fibrils of α-synuclein to gain a molecular-level insight into fibril disruption mechanisms. The results revealed that the applied external electric field induces substantial changes in the conformation of the α-synuclein fibrils. Furthermore, we show the threshold value for electric field strength required to completely disrupt the α-synuclein fibrils by opening the hydrophobic core of the fibril. Thus, our findings might serve as a valuable foundation to better understand molecular-level mechanisms of the α-synuclein fibrils disaggregation process under an applied external electric field.
淀粉样蛋白的自缔合到纤维形式被认为是神经退行性疾病(包括帕金森病(PD))发病机制中的关键因素。PD 的常见症状是无意识或无法控制的运动。α-突触核蛋白是 PD 发展的主要原因,因此一直是许多抑制和隔离其表达或有效降解它的研究的主要目标。尽管如此,迄今为止,还没有有效的、经过验证的方法来预防病理性蛋白质聚集。最近的研究提出应用外电场来打断纤维。这种方法是非侵入性的,相对于其他方法有一定的优势。我们通过对高度有毒的α-突触核蛋白纤维施加电场进行分子动力学(MD)模拟,以获得对纤维破坏机制的分子水平的深入了解。结果表明,施加的外电场会引起α-突触核蛋白纤维构象的显著变化。此外,我们还展示了通过打开纤维的疏水性核心来完全破坏α-突触核蛋白纤维所需的电场强度的阈值。因此,我们的研究结果可能为更好地理解在施加外电场下α-突触核蛋白纤维解聚过程的分子水平机制提供有价值的基础。