阿尔茨海默病中的溶血磷脂酸作用机制探讨  

The study on the mechanism of action of lysophosphatidic acid(LPA)in Alzheimer's disease

作　　者：苏裕盛 SU Yu-sheng(Medical College,Ningde Normal University,Ningde,Fujian 352101,China)

机构地区：[1]宁德师范学院医学院,福建宁德352101

出　　处：《宁德师范学院学报（自然科学版）》2021年第3期264-272,共9页Journal of Ningde Normal University(Natural Science)

基　　金：宁德师范学院引进人才项目基金(2019Y20);宁德师范学院创新团队项目基金(2019T07)。

摘　　要：溶血磷脂酸(LPA)是一种重要的生物活性脂质,在神经退行性疾病,尤其是在阿尔茨海默病(AD)中起到关键作用.LPA代谢功能异常可导致淀粉样β(Aβ)肽异常积累,神经元纤维缠结(NFT)形成,神经发炎并最终导致神经元死亡.研究发现,AD的另一个重要病理特征是神经胶质细胞的激活,CNS中星形胶质细胞和小胶质细胞的激活神经炎症是AD的1个突出特征,这可以通过反应性小胶质细胞的数量来证明.未来,若可以通过靶向LPA途径改变小胶质细胞的极化状态开发新药,将极有益于罹患AD的患者.LPA is an important bioactive lipid and plays a key role in neurodegenerative diseases, especially Alzheimer′s disease(AD). Abnormal LPA metabolism can lead to abnormal accumulation of Aβ peptide, nerve fiber tangles(NFTs) formation, nerve inflammation, and ultimately neuronal death. Studies have found that another important pathological feature of AD is the activation of glial cells, especially the activation of astrocytes and microglias in CNS, which is a prominent feature of AD, which can be proved by the number of reactive microglias.In the future, if the polarization of microglia can be changed by targeting LPA for the development of new drugs, it will be very beneficial to patients with AD.

关 键 词：溶血磷脂酸(LPA) 作用机制 阿尔茨海默病(AD) AΒ NFT TAU蛋白 神经元纤维缠结 

分 类 号：R363[医药卫生—病理学]