Peripheral and central neuroimmune mechanisms in Alzheimer's disease pathogenesis

被引:0
|
作者
Zhang, Shuo [1 ,2 ]
Gao, Yue [1 ,2 ]
Zhao, Yini [1 ,2 ]
Huang, Timothy Y. [3 ]
Zheng, Qiuyang [1 ,2 ]
Wang, Xin [1 ,2 ]
机构
[1] Xiamen Univ, Inst Neurosci,Sch Med,Affiliated Hosp 1, State Key Lab Cellular Stress Biol,Dept Neurol, Fujian Prov Key Lab Neurodegenerat Dis & Aging Res, Xiamen 361102, Fujian, Peoples R China
[2] Xiamen Univ, Shenzhen Res Inst, Shenzhen 518057, Guangdong, Peoples R China
[3] Sanford Burnham Prebys Med Discovery Inst, Neurosci Initiat, La Jolla, CA 92037 USA
基金
中国国家自然科学基金; 国家重点研发计划;
关键词
Alzheimer's disease; Peripheral immune cell; Microglia; Neuroimmune interaction; Blood-brain barrier; BETA-SPECIFIC TH1; T-CELLS; MYELOID CELLS; INFLAMMATORY MACROPHAGES; CEREBROSPINAL-FLUID; COGNITIVE DECLINE; SOLUBLE TREM2; MOUSE MODELS; PATHOLOGY; ACTIVATION;
D O I
10.1186/s13024-025-00812-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alzheimer's disease (AD) poses a growing global health challenge as populations age. Recent research highlights the crucial role of peripheral immunity in AD pathogenesis. This review explores how blood-brain barrier disruption allows peripheral immune cells to infiltrate the central nervous system (CNS), worsening neuroinflammation and disease progression. We examine recent findings on interactions between peripheral immune cells and CNS-resident microglia, forming a self-perpetuating inflammatory cycle leading to neuronal dysfunction. Moreover, this review emphasizes recent developments in the dysregulation of immune factors from both the periphery and CNS, and their impact on AD progression. With ongoing research and development of new therapeutic strategies, this review underscores the importance of modulating interactions between the peripheral immune system and CNS in AD therapy.
引用
收藏
页数:15
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