Amyloid-β oligomers in cellular models of Alzheimer's disease

J Neurochem. 2020 Nov;155(4):348-369. doi: 10.1111/jnc.15030. Epub 2020 May 18.

Abstract

Amyloid-β (Aβ) dysmetabolism is tightly associated with pathological processes in Alzheimer's disease (AD). Currently, it is thought that, in addition to Aβ fibrils that give rise to plaque formation, Aβ aggregates into non-fibrillar soluble oligomers (AβOs). Soluble AβOs have been extensively studied for their synaptotoxic and neurotoxic properties. In this review, we discuss physicochemical properties of AβOs and their impact on different brain cell types in AD. Additionally, we summarize three decades of studies with AβOs, 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 AβOs in neurons and glial cells, putatively shedding light on the development of innovative therapies for AD.

Keywords: Alzheimer's disease; amyloid-beta; cell cultures; oligomers.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Amyloid / metabolism*
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Brain / metabolism*
  • Brain / pathology
  • Cells, Cultured
  • Humans
  • Neural Stem Cells / metabolism
  • Neural Stem Cells / pathology
  • Neurons / metabolism*
  • Neurons / pathology
  • Protein Aggregation, Pathological / metabolism
  • Protein Aggregation, Pathological / pathology

Substances

  • Amyloid
  • Amyloid beta-Peptides