摘要
背景：小胶质细胞激活是神经炎症的标志，见于大多数急性和慢性神经精神病学。随着对小脑胶质细胞功能的了解，在测量大脑中进行改变，小胶质细胞激活在阿尔茨海默病（AD）的疾病进展和发病机制的背景下越来越多地被讨论。然而，基础分子机制仍然很不清楚。虽然对于其清除职责基本上需要适当的小胶质细胞功能，但脑的先天免疫细胞的局部激活也带来许多不太有利的变化，例如活性氧（ROS）产生，促炎细胞因子的分泌或神经保护性类维生素A的降解，从而不必要地将周围的健康神经元置于危险之中。鉴于这一困境，AD疫苗接种试验和免疫抑制策略在AD患者中一直失败并不奇怪。然而，流行病学证据表明对抗炎药具有保护作用，支持这样的假设，即在记忆障碍成为临床显着之前很长时间内，AD可能在疾病的时间过程中相当早地发生AD发病机制的关键过程。 小胶质细胞的激活导致严重改变的微环境。这不仅是由分泌过多的细胞因子，趋化因子或ROS引起的，而且也可能涉及神经保护内源性物质例如视黄酸（RA）的更新周转，如最近体外显示的。 结果：我们讨论了关联小胶质细胞激活和AD的发现，并推测出导致局部RA浓度在体外发生变化的小胶质细胞功能障碍可能是AD发病机制的基础，并且可以推动或促进AD发病。因此，慢性“先天性神经炎症”可能为预防和治疗策略提供有价值的目标。
关键词: 阿尔茨海默病，淀粉样蛋白β，tau，神经炎症，小神经胶质细胞，维生素A，视黄酸，视黄醇信号，小胶质细胞活化
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