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Evidence suggests that the accumulation of amyloid-beta (Aβ) peptides in the brain is an important factor in the pathophysiology of Alzheimer disease (AD). Genetic, neuropathological, and cell-biological evidence suggest that targeting Aβ could be beneficial in patients with AD. In fact, a secondary analysis of two previous trials (EXPEDITION and EXPEDITION2; Alzheimers Dement 2016; 12:110) showed that solanezumab, a humanized monoclonal antibody designed to bind to and clear soluble Aβ from the brain, significantly slowed cognitive and functional decline in patients with mild AD.
To try to replicate this finding, investigators conducted an industry-funded, randomized, double-blind, placebo-controlled, phase III trial (EXPEDITION3), in which…