Amyloid-beta oligomers in cellular models of Alzheimer's disease.

Amyloid-beta (Abeta) dysmetabolism is tightly associated with pathological processes in Alzheimer's disease (AD). Currently, it is thought that, in addition to Abeta fibrils that give rise to plaque formation, Abeta aggregates into non-fibrillar soluble oligomers (AbetaOs). Soluble AbetaOs have been extensively studied for their synaptotoxic and neurotoxic properties. In this review, we discuss physicochemical properties of AbetaOs and their impact on different brain cell types in AD. Additionally, we summarize three decades of studies with AbetaOs, providing a compelling bulk of evidence regarding cell-specific mechanisms of toxicity. Cellular models may lead us to a deeper understanding of the detrimental effects of AbetaOs in neurons and glial cells, putatively shedding light on the development of innovative therapies for AD.