Recent Aβ-immunotherapy trials have yielded the first clear evidence that removing aggregated Aβ from the brains of symptomatic patients can slow the progression of Alzheimer's disease. The clinical benefit achieved in these trials has been modest, however, highlighting the need for both a deeper understanding of disease mechanisms and the importance of intervening early in the pathogenic cascade. An immunoprevention strategy for Alzheimer's disease is required that will integrate the findings from clinical trials with mechanistic insights from preclinical disease models to select promising antibodies, optimize the timing of intervention, identify early biomarkers, and mitigate potential side effects. Recent Aβ-immunotherapy trials demonstrated that removing aggregated Aβ from the brains of symptomatic patients can slow progression of Alzheimer's disease. This perspective analyzes different immunoprevention strategies by integrating findings from clinical trials with mechanistic insights from preclinical disease models.