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About 25 years ago, β-amyloid (Aβ) clearly was shown to be neurotoxic and likely an important part of the pathogenesis of Alzheimer disease (AD). In mice, therapies that inhibited production, or sped degradation, of Aβ caused regression of plaques and improved cognitive function. However, results of multiple human trials based on “the amyloid hypothesis” have been disappointing.
In a preclinical mouse study, a new monoclonal antibody — aducanumab — was shown to enter the brain, bind selectively to Aβ in plaques, and shrink plaques. Those findings prompted this manufacturer-supported, randomized, placebo-controlled trial in 165 patients who had mild cognitive impairment or early AD and positron-emission tomographic (PET) scans positive for Aβ…