Testing this premise in an amyloid-beta-driven AD mouse model, 5XFAD29, led us to discover that transient reduction of systemic immune suppression (by reducing systemic levels of FoxP3 regulatory T cells or by blocking the inhibitory programmed-death (PD)-1 immune checkpoint pathway), could lead to Alzheimerʼs disease modification26,30. This evidence concerns the gene FOXP3 and Alzheimer disease.