In the current study, given the long-term neuroinflammation, as a central mechanism contributing to AD, induced by especially non-neurotropic IAV virus on hippocampal morphology and function (Hosseini et al., 2018), we aimed to investigate the role of H3N2 IAV infection for the development and progression of AD symptoms in an APP/PS1 transgenic mouse model. This evidence concerns the gene APP and Alzheimer disease.