Institute of Biophysics, Biological Research Centre, 6726 Szeged, Hungary.
Doctoral School of Biology, University of Szeged, 6726 Szeged, Hungary.
Cells. 2020 Jul 4;9(7):1614. doi: 10.3390/cells9071614.
Aging is characterized by a chronic low-grade sterile inflammation dubbed as inflammaging, which in part originates from accumulating cellular debris. These, acting as danger signals with many intrinsic factors such as cytokines, are sensed by a network of pattern recognition receptors and other cognate receptors, leading to the activation of inflammasomes. Due to the inflammasome activity-dependent increase in the levels of pro-inflammatory interleukins (IL-1β, IL-18), inflammation is initiated, resulting in tissue injury in various organs, the brain and the spinal cord included. Similarly, in age-related diseases of the central nervous system (CNS), inflammasome activation is a prominent moment, in which cells of the neurovascular unit occupy a significant position. In this review, we discuss the inflammatory changes in normal aging and summarize the current knowledge on the role of inflammasomes and contributing mechanisms in common CNS diseases, namely Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and stroke, all of which occur more frequently with aging.
衰老是一种以慢性低度非传染性炎症为特征的现象，这种炎症被称为炎症衰老，部分源于细胞碎片的积累。这些细胞碎片作为危险信号，与细胞因子等许多内在因素一起，被模式识别受体和其他同源受体网络感知，导致炎症小体的激活。由于炎症小体活性依赖性促炎细胞因子（IL-1β、IL-18）水平的增加，炎症被引发，导致包括大脑和脊髓在内的各种器官的组织损伤。同样，在与年龄相关的中枢神经系统（CNS）疾病中，炎症小体的激活是一个突出的时刻，其中神经血管单元的细胞占据着重要的位置。在这篇综述中，我们讨论了正常衰老过程中的炎症变化，并总结了目前关于炎症小体及其在常见 CNS 疾病（如阿尔茨海默病、帕金森病、肌萎缩侧索硬化和中风）中作用的知识，所有这些疾病在衰老过程中更为常见。
