Amyloid-β immunotherapies in mice and men

Given the compelling genetic and biochemical evidence that has implicated amyloid-β (Aβ) in the pathogenesis of Alzheimer's disease, many studies have focused on ways to inhibit Aβ production, to reverse or impede the formation of toxic forms of Aβ, or to facilitate the clearance of Aβ from the brain, in the hope of developing viable treatments for the disease. Using transgenic mouse models of Alzheimer's disease, many advances have been made in methodologies using different immunization techniques designed to clear soluble and aggregated forms of Aβ from the brain. We have highlighted how data derived from studies using transgenic mouse models have shaped our understanding of immunization-dependent Aβ clearance mechanisms and how these studies have influenced the development of anti-Aβ immunotherapies in humans.