本文已被:浏览 809次 下载 2488次
Received:December 03, 2022 Published Online:May 20, 2023
Received:December 03, 2022 Published Online:May 20, 2023
中文摘要: 阿尔茨海默病(AD)神经炎症的发病机制和治疗靶点是研究的热点,β型肾上腺素能受体(β-AR)可调节AD发病过程中的神经炎症。β-AR在中枢神经系统固有免疫细胞(小胶质细胞和星形胶质细胞)、血脑屏障以及外周免疫细胞均有表达,可激动上述细胞和结构中的β-AR来抑制神经炎症。本文阐述β-AR在AD神经炎症中的作用,并总结β-AR激动剂与阻滞剂在AD神经炎症中的相关研究进展,旨在为AD发病机制和治疗靶点研究提供新的思路。
Abstract:The pathogenesis and therapeutic targets of neuroinflammation in Alzheimer‘s disease(AD) are hot research topics. β-adrenergic receptors(β-AR) can regulate neuroinflammation during the pathogenesis of AD. β-AR is expressed in innate immune cells(microglia and astrocytes) of the central nervous system, blood brain barrier, and peripheral immune cells, which can stimulate the expression of AR in these cells and structures to suppress neuroinflammation. The review describes the role of β-AR in neuroinflammation in AD, and summarizes the studies of β-AR agonists and blockers in neuroinflammation, aiming to provide a new idea for pathogenesis and therapeutic target research of AD in future.
keywords: Alzheimer‘s disease β-adrenergic receptor Neuroinflammation Blood brain barrier Immune cell β-amyloid
文章编号: 中图分类号:R742 文献标志码:A
基金项目:辽宁省科学技术计划项目(辽科发2022-54-77);沈阳市科学技术计划项目(20-205-4-050)
引用文本: