神经炎症
小胶质细胞
疾病
神经科学
炎症
炎症体
趋化因子
生物
载脂蛋白E
阿尔茨海默病
转录组
多发性硬化
星形胶质细胞
促炎细胞因子
脂类学
中枢神经系统
神经退行性变
免疫学
串扰
医学
老年斑
血脑屏障
陶氏病
信号转导
作者
A. K. Kakkar,Harpreet Singh,Bhuvnesh Kumar Singh,Arvind Kumar,Arun Kumar Mishra,Hitesh Chopra
标识
DOI:10.1177/13872877251374353
摘要
Alzheimer's disease (AD), the most prevalent form of dementia, is pathologically defined by amyloid-β (Aβ) plaques, neurofibrillary tangles, synaptic loss, and progressive neuronal degeneration. Increasing evidence highlights neuroinflammation as a central and modifiable factor in AD pathogenesis. This review critically explores the roles of microglia and astrocytes in mediating neuroinflammatory cascades, emphasizing their dual protective and detrimental functions. Microglial activation and astrocytic polarization into A1 (neurotoxic) and A2 (neuroprotective) subtypes are discussed alongside their contributions to Aβ clearance, tau pathology propagation, and synaptic dysfunction. The disruption of the blood–brain barrier, activation of inflammasome pathways such as NLRP3, and release of cytokines and chemokines exacerbate chronic inflammation and neurodegeneration. Advances in single-cell transcriptomics and lipidomics have revealed glial heterogeneity and novel molecular targets, including disease-associated microglia. Genetic risk factors like apolipoprotein E ( APOE ) and TREM2 variants further modulate inflammatory responses. Emerging therapeutic strategies, including non-steroidal anti-inflammatory drugs, monoclonal antibodies, and targeted immunomodulators, hold promise for modifying disease progression. Overall, precise targeting of neuroinflammatory pathways offers a compelling avenue for future AD therapies.
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