New neurons are continuously added to the subgranular zone of the hippocampus throughout the lifespan, but the functional consequences of hippocampal neurogenesis remain unclear. While the majority of previous studies have examined the impact of increasing or decreasing hippocampal neurogenesis on subsequent memory formation, few have examined the effects of similar manipulations on established, hippocampus-dependent memories. Computational models predict that addition of new neurons should lead to extensive remodeling of hippocampal circuits, and consequently degradation or forgetting of established memories. Consistent with this, lifespan changes in hippocampal neurogenesis are inversely correlated with memory persistence: During infancy, when hippocampal neurogenesis levels are high, freshly-generated memories tend to be rapidly forgotten. In contrast, during adulthood, when neurogenesis levels are lower, memories are typically much more persistent. We have conducted two types of experiments that suggest that neurogenesis and forgetting are causally related. First, in adult mice (P60), we find that increasing neurogenesis after memory formation is sufficient to induce forgetting. Second, in infant mice (P17), we find that decreasing neurogenesis after memory formation mitigates normal forgetting observed at this age. Our data suggest a causal relationship between neurogenesis and memory persistence, and provide a neurobiological account for infantile amnesia.