中山大学学报（医学科学版）2025，Vol.46Issue(6)：973-984,12.
C反应蛋白在阿尔茨海默病炎症与淀粉样毒性中的关联性研究进展
Research Advances in the Association Between Inflammation and Amyloid Toxicity in Alzheimer's Disease
摘要
Abstract
Amyloid-β peptide(Aβ)is considered a major cause of Alzheimer's disease(AD).However,current researches emphasize that Aβ can activate microglia and astrocytes,which causes neuroinflammation.Neuroinflammation plays a crucial role in the neuronal mortality process,and can be considered the underlying cause of AD.In addition,vascular damage was proposed to play an important role in the pathogenesis of AD more than two decades ago,but few researchers have focused on the positive role of cerebrovascular damage in AD.In recent years,a growing body of evidence has supported that brain microvascular injury causes the occurrence of AD.Moreover,recent research indicated that inflammation caused by brain microvascular injury is also a significant risk factor for the development of AD.In damaged microvessels,C-reactive protein(CRP)is a non-specific inflammatory marker,which can activate the complement and enhance phagocytosis of immune cells,and help to eliminate pathogenic microorganisms from the body.The plenty of evidence indicated that CRP penetrated brain tissue and participated in neuroinflammation during brain microvascular injury,thereby influencing the pathogenesis of AD.Therefore,the negative effects of CRP and Aβ on the pathogenesis of AD are equally important.At present,few researchers have established a link between the effects of CRP and Aβ on AD and conducted in-depth analysis.This article firstly and deeply analyzed and summarized the significant function and connection of Aβ and CRP in AD,which provided support for the theory that neuronal cerebrovascular injury is the cause of AD.关键词
C-反应蛋白/β淀粉样蛋白/阿尔茨海默病/炎症/微血管损伤Key words
C-reactive protein/amyloid-β peptide/Alzheimer'disease/inflammation/microvascular injury分类
医药卫生引用本文复制引用
张洁,朱益宜..C反应蛋白在阿尔茨海默病炎症与淀粉样毒性中的关联性研究进展[J].中山大学学报（医学科学版）,2025,46(6):973-984,12.基金项目
西藏自治区自然科学基金(XZ202501ZR0080) （XZ202501ZR0080）
