CRMP2磷酸化参与阿尔茨海默病的机制研究进展

AResearch progress on the mechanism of CRMP2 phosphorylation in Alzheimer′s disease

阿尔茨海默病(Alzheimer's disease,AD)是一种常见神经系统退行性疾病。脑衰反应调节蛋白2(collapsin response mediator protein2,CRMP2)在AD病变进展中发挥作用,CRMP2高磷酸化导致神经元轴突末端微管稳定性下降,神经元轴浆运输异常,从而导致神经元线粒体动力学异常,抑制溶酶体自噬能力,导致NMDA受体过度激活。CRMP2磷酸化为AD药物研发提供了思路。本文就有关CRMP2参与AD病变的相关分子机制的研究进展进行综述,以期为靶向药物的研发提供参考资料。

Alzheimer's disease(AD)is a common neurological degenerative disease.Collapsin response mediator protein2(CRMP2)plays an important role in the progression of AD.Hyperphosphorylation of CRMP2 results in decreased stability of axonal terminal microtubules and abnormal axoplasmic transport of neurons,which leads to abnormal mitochondrial dynamics of neurons,inhibits the ability of lysosomal autophagy,and leads to excessive activation of NMDA receptors.The phosphorylation of CRMP2 provides a new idea for AD drug develop⁃ment.In this review,the molecular mechanisms of CRMP2 involved in AD are reviewed,which can provide refer⁃ences for the development of targeted drugs.