Xie Jingdun, Wang Haitao, Lin Ting, Bi Bingtian
Department of Anesthesiology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou 510060, China.
Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China.
Biomed Res Int. 2017;2017:2986460. doi: 10.1155/2017/2986460. Epub 2017 Apr 3.
The main hallmarks of Alzheimer's disease (AD) are extracellular deposits of amyloid plaques and intracellular accumulation of hyperphosphorylated neurofibrillary tangles (tau). However, the mechanisms underlying these neuropathological changes remain largely unclear. To date, plenty of studies have shown that microglia-mediated neuroinflammation contributes to the pathogenesis of AD, and the microglia-synapse pathways have been repeatedly identified as the crucial factor in the disease process. In this review, evidences from microglia and synapse studies are presented, and the role of microglia in the pathogenesis of AD, the contributing factors to synapse dysfunction, and the role and mechanisms of microglia-synapse pathways will be discussed.
阿尔茨海默病(AD)的主要特征是细胞外淀粉样斑块沉积和细胞内过度磷酸化神经原纤维缠结(tau)的积累。然而,这些神经病理变化背后的机制在很大程度上仍不清楚。迄今为止,大量研究表明,小胶质细胞介导的神经炎症促成了AD的发病机制,并且小胶质细胞-突触途径已被反复确认为疾病过程中的关键因素。在这篇综述中,将呈现来自小胶质细胞和突触研究的证据,并讨论小胶质细胞在AD发病机制中的作用、突触功能障碍的促成因素以及小胶质细胞-突触途径的作用和机制。