Alzheimer’s Disease (AD) is pathologically characterized by the accumulation of soluble oligomers causing extracellular beta-amyloid deposits in form of neuritic plaques and tau-containing intraneuronal neurofibrillary tangles in brain. One proposed mechanism explaining the formation of these proteins is impaired phagocytosis by microglia/macrophages resulting in defective clearance of soluble oligomers of beta-amyloid stimulating aggregation of amyloid plaques subsequently causing AD. However, research indicates that activating macrophages in M2 state may reduce toxic oligomers. NEU1 mutation is associated with a rare disease, sialidosis. NEU1 deficiency may also cause AD-like amyloidogenic process. Amyloid plaques have successfully been reduced using NEU1.Thus, NEU1 is suggested to have therapeutic potential for AD, with lysosomal exocytosis being suggested as underlying mechanism. Studies however demonstrate that NEU1 may activate macrophages in M2 state, which as noted earlier, is crucial to reducing toxic oligomers. In this review, authors discuss the potential therapeutic role of NEU1 in AD via immune system.

阿尔茨海默氏病 (AD) 的病理特征是可溶性低聚物的积累，导致细胞外 β-淀粉样蛋白以神经炎斑块和大脑中含有 tau 的神经元内神经原纤维缠结的形式沉积。解释这些蛋白质形成的一种提出的机制是小胶质细胞/巨噬细胞的吞噬作用受损，导致β-淀粉样蛋白可溶性低聚物的清除缺陷，刺激淀粉样蛋白斑块聚集，随后引起AD。然而，研究表明，激活 M2 状态的巨噬细胞可能会减少有毒的寡聚物。 NEU1 突变与一种罕见疾病——唾液酸贮积症有关。 NEU1 缺乏也可能导致 AD 样淀粉样变过程。使用 NEU1 已成功减少淀粉样斑块。因此，NEU1 被认为具有治疗 AD 的潜力，溶酶体胞吐作用被认为是潜在机制。然而研究表明，NEU1 可能会激活 M2 状态的巨噬细胞，如前所述，这对于减少有毒寡聚物至关重要。在这篇综述中，作者讨论了 NEU1 通过免疫系统在 AD 中的潜在治疗作用。