The etiology of most neurodegenerative diseases remains unknown. Viral infections have been associated with the risk of developing Alzheimer’s disease; however, a detailed causal relationship has yet to be identified. Here we show that a transient viral infection of the body increases the presence of T cells, an immune cell that usually attacks tumor cells or viruses, in the noninfected brain and at its borders. In a mouse model of Alzheimer’s disease, infiltrating T cells were spatially associated with areas affected by abnormal levels of amyloid beta protein depositions. Our proposal aims at understanding if, and how, various forms of T cells generated after a viral infection influence brain pathology during states of neurodegeneration. We hope to find clues from sophisticated animal studies that could not otherwise be obtained from patients. These results may potentially change the course of Alzheimer’s disease by targeting the antiviral immune response when the pathogen is no longer a threat.