β淀粉样蛋白所致的炎症反应在阿尔茨海默病中的作用机制

摘要

阿尔茨海默病（ AD）是一种慢性神经退行性疾病，β淀粉样蛋白（ Aβ）在海马过度沉积形成的老年斑是其主要的病理特点。 Aβ激活胶质细胞介导的炎症反应分泌促炎因子包括白细胞介素1、白细胞介素6及肿瘤坏死因子α等可以导致神经细胞变性、损伤和死亡。 Aβ也可通过与 Tau蛋白相互作用介导的炎症反应加快 AD的进展。因此，Aβ沉积激活胶质细胞引起的炎症反应可能是AD的重要致病机制。%Alzheimer′s disease ( AD ) is a chronic neurodegenerative diseases, with senile plaques formed byβ-amyloid( Aβ) excessive deposition in the hippocampus as one of the main pathological features . Aβactivation of glial cell-mediated inflammatory response secrets proinflammatory cytokines including inter-leukin-1,tumor necrosis factor-αand interleukin-6 and result in nerve cell damage,degeneration and death. Aβand Tau protein interaction may also accelerate the progression of AD .Therefore,inflammation caused by inflammation activated by Aβdeposits may be an important pathogenic mechanism of AD .