APP and Alzheimer disease: Taken together, our data firstly uncover an abnormally upregulated circRNA, circDlg1 in the microglia of both AD patients and APP/PS1 mice and subsequently emphasize that microglia-specific knockdown of circDlg1 or the downstream effector molecule PDE4B is sufficient to maintain microglial protective response, restrain the pro-inflammatory gene program, and mitigate neuroinflammation of AD mice, thus pushing the frontier understanding of cell-specific regulation by circRNA in the microglia of AD.