Mechanism of secondary nucleation from the direct observation of Aβ42 aggregation at the single fibril level

The formation of amyloid fibrils and oligomers is linked to several neurodegenerative disorders, including Alzheimer’s disease (AD). To tackle these diseases, we need to progress our understanding at the molecular level, including the determination of the mechanisms and rates of fibril formation and self-replication. In the context of AD, the facilitation of the formation of new Aβ42 fibrils by existing ones through secondary nucleation is a major source of both new fibrils and toxic oligomeric species.