Amyloid-β immunotherapies in mice and men

Given the compelling genetic and biochemical evidence that has implicated amyloid-beta (A beta) in the pathogenesis of Alzheimer's disease, many studies have focused on ways to inhibit AD production, to reverse or impede the formation of toxic forms of AD, or to facilitate the clearance of AD 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 AD from the brain. We have highlighted how data derived from studies using transgenic mouse models have shaped our understanding of immunization-dependent AD clearance mechanisms and how these studies have influenced the development of anti-A beta immunotherapies in humans.