摘要
大量研究报告显示,糖原合成酶激酶-3(glycogen synthase kinase3,GSK3)在阿尔茨海默病(Alzheimer s dis-ease,AD)发病机制中起着重要的作用。AD患者存在GSK3活性的增强和水平的提高。细胞培养、无脊椎动物和哺乳类动物模型研究发现,GSK3活性增强导致tau的过度磷酸化、Aβ产生的增加、学习和记忆能力的缺损,同时伴有神经退行性变。GSK3抑制剂能防止AD转基因动物tau的过度磷酸化,使得GSK3抑制剂有望用于预防和治疗AD。
Multiple reports suggest that glycogen synthase kinase-3 （GSK3） plays an important role in the pathogenesis of Alzheimer＇s disease （ AD）. The level and enzymatic activity of GSK3 is elevated in AD. Cell culture studies and animal model studies with both invertebrates and mammals find that over-activity of GSK3 causes hyper-phosphorylation of the tau protein, increased production of β-amyloid, learning and memory impairments, and associated neurodegeneration. GSK-3β inhibitors prevent tau hyper-phosphorylation in AD transgenic animals so they are of potential use in the prevention and treatment of AD.
出处
《上海精神医学》
2011年第4期233-236,共4页
Shanghai Archives of Psychiatry
