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S1-Apecs Trial of the Bace1 Inhibitor Verubecestat for Prodromal Alzheimer’S Disease. Jeffrey L. Cummings (Cleveland Clinic, Las Vegas, NV, USA)

Introduction: The amyloid hypothesis proposes that Aβ peptides are intimately involved in the etiology of Alzheimer’s disease (AD) via their aggregation to form toxic complexes that lead to neurodegeneration. Aβ is produced via sequential proteolytic cleavage of the parent molecule, amyloid precursor protein, by β-secretase (BACE1) followed by γ-secretase. Inhibition of BACE1 is a potential novel therapeutic strategy for slowing or halting progression of AD by reducing Aβ production. This approach differs from previous anti-amyloid approaches using monoclonal antibodies to clear Aβ. In the first large-scale clinical trial (EPOCH) of a BACE1 inhibitor, verubecestat doses of 12 mg and 40 mg were ineffective at slowing the rate of cognitive or functional decline over 78 weeks in participants with clinically diagnosed mild-to-moderate AD, despite...

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