Alzheimer's disease is a neurodegenerative disease with hidden onset, and the cause of the disease has not been determined yet. At present, there is no effective cure method or drug in clinic. With the deepening of research, scientists have made new progress in effective methods and drugs to treat the disease. Recently, the team of Professor Wang Yifei from the cell line of the School of Life Science and Technology of Jinan University revealed that microglia of Alzheimer's disease highly express Mamdc2 gene, which promotes the innate antiviral immunity induced by microglia infected by neurotropic virus, providing new clues to understand the mechanism of the relationship between Alzheimer's disease and herpes simplex virus type 1. Relevant research results were published in the Journal of Infectious Diseases. The immune response of microglia is related to Alzheimer's disease. According to the study on the global burden of disease published by the Lancet in 2016, Alzheimer's disease ranks eighth in the burden of disease in China. "The pathogenesis of Alzheimer's disease is still unknown globally. Its treatment methods are extremely limited, and drug development has failed." Wang Yifei said. Human herpes simplex virus (HSV) is a common pathogen in human body, which includes two serotypes: herpes simplex virus type 1 and herpes simplex virus type 2. Wang Yifei's team has studied herpes virus for more than 20 years. "It was originally believed that herpes virus was not harmful to human body, but in recent years, a large number of studies have shown that herpes simplex virus type 1 infection plays a certain role in neurodegenerative diseases." Wang Yifei introduced. "HSV-1 is the most common human neurotropic virus closely related to Alzheimer's disease, and its infection can cause herpes simplex encephalitis. However, the mechanism of association between HSV-1 and Alzheimer's disease is still unclear." Wang Yifei said, "Therefore, it is of great significance to clarify the mechanism of action between herpes simplex virus type 1 and Alzheimer's disease." It is reported that microglia, as macrophages of the central nervous system, are the key line of defense against neurotropic virus infection. Once herpes simplex virus type 1 infects microglia, microglia will produce immune response, and its excessive secretion of brain type I interferon can cause neuroinflammation, which may increase the risk of Alzheimer's disease. To provide new research ideas and clues for the treatment of Alzheimer's disease Wang Yifei's team screened the highly expressed gene Mamdc2 in microglia of Alzheimer's disease model mice and herpes simplex virus type 1 infected mice by analyzing the single cell transcriptome data of microglia of Alzheimer's disease model mice. "This is a key gene. Molecular mechanism studies have found that Mamdc2 interacts with STING through its first MAM domain, enhances the polymerization of STING, and promotes the activation of type I interferon in the brain mediated by TBK1-IRF3 signaling pathway." Wang Yifei pointed out that these results indicate that Mamdc2 promotes the antiviral natural immune response of microglia by regulating the polymerization of STING. "Our research clarifies the role of Mamdc2, indicating that Mamdc2 is a possible link between herpes simplex virus type 1 infection and the pathogenesis of Alzheimer's disease