Abstract Alzheimer’s disease (AD) is a neurodegenerative disorder that is characterized by the accumulation of amyloid-beta (Aβ) aggregates, in the form of fibrils and plaques. While it has largely been stated that Aβ oligomers are the main toxic species, significant evidence indicates that fibrils may also be relevant to AD pathogenesis. Notably, evidence indicates that while fibrils, through direct interaction with neuronal membranes, contribute to synaptic dysfunction and cellular damage, no