CAJ | 학술논문

本文分析了阿尔采末病（ AD）的病理机制，对肝素类药物神经保护机制的进展进行了综述。阐明了肝素类药物可通过调节IP3受体介导的细胞内钙释放，影响淀粉样蛋白（ Aβ）沉积及其毒性、调节tau蛋白的磷酸化状态，保护胆碱能神经元等发挥神经保护作用，从而延缓AD的发生与发展。
본문분석료아이채말병（ AD）적병리궤제，대간소류약물신경보호궤제적진전진행료종술。천명료간소류약물가통과조절IP3수체개도적세포내개석방，영향정분양단백（ Aβ）침적급기독성、조절tau단백적린산화상태，보호담감능신경원등발휘신경보호작용，종이연완AD적발생여발전。
This paper analyzed the pathological mechanisms of AD,reviewed the progress of the mechanisms of the neu-roprotective effect of heparin and its derivatives,clarified that heparin and its derivatives had neuroprotective effects through regulating IP3Rs-mediated intracellular calcium release,inhibiting Aβdeposition and Aβ-induced toxicity,regulating the tau protein phosphorylation state,and protecting cholinergic neurons,thereby delayed the occurrence and development of AD.