The amyloid hypothesis of Alzheimer's disease (AD) maintains that the accumulation of the amyloid β protein (Aβ) is a critical event in disease pathogenesis. A great deal of both academic and commercial research has focused on the mechanisms by which Aβ is generated. However, investigations into the mechanisms underlying Aβ clearance have blossomed over the last several years. This minireview will summarize pathways involved in the removal of cerebral Aβ, including enzymatic degradation and receptor-mediated efflux out of the brain.