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A more pathological amyloid-β oligomer

Amyloid-β (Aβ) is implicated in the pathology of Alzheimer’s disease (AD), and various types of Aβ oligomers emerge at different stages of AD. Aβ promotes the modification and aggregation of the microtubule-associated protein tau, which is associated with neuronal toxicity and impaired cognition in various neurodegenerative disorders. Using several transgenic mouse models of AD and cultured cortical neurons, Amar et al. found that the 56-kDa oligomer Aβ*56, but not Aβ dimers or trimers, stimulated an influx in intracellular Ca2+ that triggered phosphorylation of tau at a site that promoted its aggregation. The findings link a specific amyloid form to tau pathology and suggest that dissecting the molecular and stage-specific roles of Aβ oligomers may lead to improved therapies.