Microglia, the immune cells of the central nervous system, are long lived. In mice, microglia have an average lifespan of 15.5 months. When microglia are experimentally depleted from the mouse brain, microglia populations quickly return to steady state levels. The mechanisms of this observed repopulation are unclear. More importantly, the mechanisms of microglia replenishment in the healthy brain are not well understood. The literature supports two competing hypotheses. One is that microglia proliferate simply by dividing. Another possibility is that pools of microglia progenitor cells within the central nervous system divide and differentiate into microglia. I hypothesize that microglia proliferate primarily through the differentiation of progenitor cells. Available data to date suggest CD133 as a potential marker for microglia progenitor cells. In order to study these putative progenitor populations, I used a genetic reporter mouse line in which administration of tamoxifen induces TdTomato expression specifically in CD133-expressing cells. TdTomato, a red fluorescent protein, allows these cells to be visualized under a fluorescence microscope. Importantly, all the progeny of these cells also express TdTomato, allowing us to determine whether CD133 cells generate new microglia over time. After tamoxifen treatment at the age of 10 weeks, mice were sacrificed at three and nine months of age. Brains were fixed, sectioned, and labeled with antibodies to a microglia specific protein and to TdTomato. Daughter microglia that differentiated from CD133-expressing cells express both markers. Using a fluorescence microscope, I identified several microglia daughter cells of CD133-expressing cells. This suggests that microglia populations replenish in the healthy brain at least in part through the division of CD133-expressing cells. We can apply this new knowledge about how new microglia are generated in the healthy mouse brain to further our understanding of how microglia population dynamics are affected in both health and disease.