Abstract：
Alzheimer\'s disease (AD) is distinguished by extracellular accumulation of amyloid-beta plaques and intracellular neurofibrillary tangles of Tau. Pathogenic Tau species are also known to display \"prion-like propagation,\" which explains their presence in extracellular spaces as well. Glial population, especially microglia, tend to proclaim neuroinflammatory condition, disrupted signaling mechanisms, and cytoskeleton deregulation in AD. Omega-3 fatty acids play a neuroprotective role in the brain, which can trigger the anti-inflammatory pathways as well as actin dynamics in the cells. Improvement of cytoskeletal assembly mechanism by omega-3 fatty acids would regulate the other signaling cascades in the cells, leading to refining clearance of extracellular protein burden in AD. In this study, we focused on analyzing the ability of α-linolenic acid (ALA) as a regulator of actin dynamics to balance the signaling pathways in microglia, including endocytosis of extracellular Tau burden in AD.
摘要：
阿尔茨海默病（AD）的特征是β淀粉样蛋白斑块的细胞外积累和Tau的细胞内神经原纤维缠结。致病性Tau物种也被认为表现出“朊病毒样繁殖”，“这也解释了它们在细胞外空间的存在。Glialpopulation,尤其是小胶质细胞,倾向于宣布神经炎症，中断的信号机制，和AD中的细胞骨架失调。Omega-3脂肪酸在大脑中发挥神经保护作用，这可以触发细胞中的抗炎途径以及肌动蛋白动力学。ω-3脂肪酸对细胞骨架组装机制的改善将调节细胞中的其他信号级联，导致AD细胞外蛋白负荷的精制清除。在这项研究中,我们专注于分析α-亚麻酸（ALA）作为肌动蛋白动力学调节剂平衡小胶质细胞信号通路的能力，包括AD细胞外Tau负荷的内吞作用。
