The neuroinflammatory interleukin-12 signaling pathway drives Alzheimer's disease-like pathology by perturbing oligodendrocyte survival and neuronal homeostasis

Central in AD-related neuroinflammation is the proinflammatory interleukin-12 (IL-12)/IL-23 signaling pathway whose inhibition has been shown to attenuate pathology and cognitive defects in AD-like mice. In order to explore which cell types are involved in this neuroinflammatory cascade, we used single-nuclei RNA sequencing in AD-like APPPS1 mice lacking or harboring IL-12/IL-23 signaling. Single-nuclei RNAseq of FACs sorted nuclei extracted from snap frozen mouse hippocampus of 250 day old animals

促炎性白细胞介素-12（interleukin-12, IL-12）/IL-23信号通路是阿尔茨海默病（Alzheimer's Disease, AD）相关神经炎症的核心通路，已有研究表明，抑制该通路可减轻类AD模型小鼠的病理损伤与认知功能缺陷。为探究参与该神经炎症级联反应的细胞类型，本研究对缺失或保留IL-12/IL-23信号通路的类AD模型APPPS1小鼠开展单核RNA测序（single-nuclei RNA sequencing, snRNA-seq）。本研究的测序样本取自250日龄小鼠的快速冷冻海马组织，通过荧光激活细胞分选（Fluorescence-Activated Cell Sorting, FACS）分离获取细胞核后进行测序。