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The increasing prevalence of Alzheimer's disease represents a global challenge at multiple levels: personal, social, and economic. The amyloid hypothesis1 posits that deposition of amyloid-beta (Aβ) in brain parenchyma is an early critical event in Alzheimer's disease that promotes or accelerates downstream features of the disease such as tangle formation, neuronal loss, and progressive dementia. Most pharmaceutical companies seeking disease-modifying treatments for Alzheimer's disease have investigated Aβ-centric therapeutics.This issue of the Journal contains reports on the phase 3 trials in Alzheimer's disease of two anti-Aβ antibodies: bapineuzumab2 and solanezumab.3 Each agent was tested in two trials. Both sets of . . .
Karran et al. (Wed,) studied this question.