淀粉样蛋白的沉积与Tau蛋白磷酸化是阿尔茨海默病发病的关键分子机制,神经元胞内钙离子的变化可影响其生成和代谢;另一方面,这些蛋白的改变会进一步导致神经元钙稳态的失调,致使突触损伤、神经细胞凋亡及认知功能下降。本文就神经元钙稳态失衡在阿尔茨海默病发病中的进展进行综述。
Accumulation of amyloid-beta protein and hyperphosphorylation of microtubule-associated protein tau are two critical mechanisms in the pathogenesis of Alzheimer's disease. The metabolism and production of these two pathological proteins may be affected by altered neuronal calcium homeostasis. On the other hand, events downstream from the alteration of these pathological proteins may further exacerbate calcium dysregulation, causing synaptic dysfunction, cell apoptosis and reduction of cognition function. This review summarized the progress of unbalanced calcium homeostasis in the pathogenesis of Alzheimer's disease.