The generation of amyloid-beta peptide (Aβ) and its accumulation in amyloid plaques are generally recognized as key characteristics of Alzheimer's disease. A number of reports have indicated that Aβ can regulate the proliferation of neural precursor cells and adult neurogenesis, suggesting that this may underpin the cognitive decline and compromised olfaction also associated with the condition. Here we report that Aβ_1–42 treatment both in vitro and in vivo, as well as endogenous generation of Aβ in C100 and APP/PS1 transgenic models of Alzheimer's disease, stimulate neurogenesis of young adult subventricular zone precursors. The neurogenic effect of Aβ_1–42 was found to require expression of the p75 neurotrophin receptor (p75^NTR) by the precursor cells, and activation of p75^NTR by metalloprotease cleavage. However, precursors from 12-month-old APP/PS1 mice failed to respond to Aβ_1–42. Our results suggest that overstimulation of p75^NTR-positive progenitors during early life might result in depletion of the stem cell pool and thus a more rapid decline in basal neurogenesis. This, in turn, could lead to impaired neurogenic function in later life.