It might thus be that the interplay between pro-inflammatory cytokines and SERT function requires conditions of severe neuroinflammation, such as those encountered in murine models of experimental stroke, where the brain levels of IL-1β and TNF exceed those measured in 20-month-old APPswe/PS1dE9 mice by ~ 3–20 times, respectively [42]. This evidence concerns the gene SLC6A4 and Stroke.