Neurogenesis, the production of new neurons from neural stem cells, dramatically decreases during aging concomitantly with increased inflammation both systemically and in the brain. However, the precise role of inflammation and whether local or systemic factors drive the neurogenic decline during aging is poorly understood. Here, we identify CXCR5/5/CXCL13 signaling as a novel regulator of neurogenesis in the aged brain. The chemokine Cxcl13was found to be upregulated in the brain during aging. Loss of its receptor, Cxcr5, led to increased proliferation and decreased numbers of neuroblasts in the aged subventricular zone (SVZ), together with accumulation of neuroblasts in the rostral migratory stream and olfactory bulb (OB), without increasing the amount of new mature neurons in the OB. The effect on proliferation and migration was specific to neuroblasts and likely mediated through increased levels of systemic IL‐6 and local Cxcl12expression in the SVZ. Our study raises the possibility of a new mechanism by which interplay between systemic and local alterations in inflammation regulates neurogenesis during aging. Subventricular zone (SVZ) neuroblasts migrate along the rostral migratory stream (RMS) until they reach the olfactory bulb (OB) where they differentiate into new neurons. Aged Cxcr5−/−neuroblasts increase their proliferation and migration to accumulate in RMS/OB without increasing number of new neurons. This is likely due to increased systemic IL‐6 and Cxcl12in the SVZ, indicating that combinations of systemic and local mediators regulate neurogenic decline during aging.