The pathophysiology of Alzheimer’s disease (AD) is complex. The characteristic feature of AD is the appearance of extracellular amyloid-beta (Aβ) plaques. Many companies investigated anti-amyloid-β agents and after repeated failures, there was a shift to anti-tau therapies. The recent FDA approval of anti-amyloid therapy in nearly two decades and anti-tau failures indicates an acceptance of the hypothesis in favor of Aβ plaques. In this digest, we have highlighted the recent advances with anti-amyloid-β approaches and how the anti-tau therapies have failed