Abstract：
Neurodegenerative diseases (NDDs) pose a significant issue in healthcare, needing a thorough knowledge of their complex molecular mechanisms. A diverse set of cell signaling mediators and their interactions play critical roles in neuroinflammation. The release of pro-inflammatory mediators in response to neural dysfunction is detrimental to normal cell survival. Moreover, the important role of nuclear factor-κB (NF-κB) in the central nervous system through Toll-like receptor (TLR) activation has been well established. Therefore, through a comprehensive review of current research and experimentation, this investigation elucidates the interactions between novel pharmacological agents (TLR-4/NF-κB inhibitors) and neurodegeneration encompassing Alzheimer\'s, Parkinson\'s, Huntington\'s disease, amyotrophic lateral sclerosis and stroke. Insights garnered from this exploration underscore the potential of TLR-4 as a therapeutic target. Through the revelation of these insights, our aim is to establish a foundation for the development of enhanced and focused therapeutic approaches in the continuous endeavor to combat neurodegeneration. This review thus serves as a roadmap, guiding future research endeavors toward innovative strategies for combatting the complex interplay between TLR-4 signaling and NDDs.
摘要：
神经退行性疾病(NDDs)在医疗保健领域是一个重要问题，需要全面了解它们复杂的分子机制。一组不同的细胞信号传导介质及其相互作用在神经炎症中起关键作用。响应于神经功能障碍的促炎介质的释放对正常细胞存活是有害的。此外，核因子-κB（NF-κB）通过Toll样受体（TLR）激活在中枢神经系统中的重要作用已得到证实。因此,通过对当前研究和实验的全面回顾，这项研究阐明了新型药物（TLR-4/NF-κB抑制剂）和神经变性之间的相互作用，包括阿尔茨海默病，帕金森,亨廷顿病,肌萎缩侧索硬化症和中风。从这种探索中获得的见解强调了TLR-4作为治疗靶标的潜力。通过这些见解的启示,我们的目标是在不断努力对抗神经变性的过程中，为发展增强和集中的治疗方法奠定基础。因此，这一审查作为一个路线图，指导未来的研究努力，以创新策略来对抗TLR-4信号传导和NDD之间的复杂相互作用。
