In AD, Aβ peptides, derived from amyloid precursor protein (APP), aggregate into neurotoxic oligomers, particularly Aβ42, which self-aggregate into extracellular plaques [1, 3, 24–27] (Fig. 2), which disrupt synapses and activate microglia, which attempt to clear them but often fail [28, 29]. Here, APP is linked to Alzheimer disease.