In two phase 3 trials in patients with Alzheimer's disease, bapineuzumab, a humanized anti–amyloid-beta monoclonal antibody, did not improve clinical outcomes. Amyloid-related edema was more likely to develop in patients treated with bapineuzumab. Alzheimer's disease, a neurodegenerative disease resulting in progressive dementia, is characterized by neuropathological changes that include intraneuronal neurofibrillary tangles and extracellular neuritic plaques. The predominant component of plaques is the amyloid-beta (Aβ) peptide. Multiple lines of evidence indicate that aberrant Aβ production or clearance is an early component in the pathogenesis of Alzheimer's disease. 1 – 3 Bapineuzumab is a humanized N-terminal–specific anti-Aβ monoclonal antibody in clinical development for the treatment of Alzheimer's disease. In preclinical studies, the murine form of the antibody (3D6) was shown to bind to fibrillar, oligomeric, and monomeric forms of Aβ, reduce the amount of Aβ in . . .