Cited by 116Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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

Fontana, Igor C., Zimmer, Aline R., Rocha, Andreia S., Gosmann, Grace, Souza, Diogo O., Lourenco, Mychael V., Ferreira, Sergio T., Zimmer, Eduardo R.·2020·Journal of Neurochemistry

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.

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Crossref · 10.1111/jnc.15030

Cites

226 of 226 references verified0 citation errors · 0 not checkable

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  • Misfolded Aβ and tau proteins accumulate in the AD brain in a neurodegenerative cascade leading to cognitive decline and dementia.

    “Misfolded Aβ and tau proteins accumulate in the AD brain in a neurodegenerative cascade leading to cognitive decline and dementia [4,5,6,7,8,9].”
  • Elevated levels of Aβ oligomers are associated with AD, as they are found in AD brains and are considered the most toxic and pathogenic form of Aβ.

    “Elevated levels of oligomers have been associated with AD, as they are found in AD brains and are considered the most toxic and pathogenic form of Aβ [4,5,6,7,18].”
  • The Aβ oligomer hypothesis, supported by in vitro, in vivo, and ex vivo models, points to toxic Aβ oligomers rather than amyloid plaques as key players in AD pathogenesis.

    “The Aβ oligomer hypothesis, supported by in vitro, in vivo, and ex vivo models, points to the toxic Aβ oligomers rather than amyloid plaques as key players in AD pathogenesis [4,5,6,7].”
  • The Aβ oligomer hypothesis points to toxic Aβ oligomers rather than amyloid plaques as key players in Alzheimer's disease pathogenesis.

    “The alternative “Aβ oligomer hypothesis”, supported by in vitro, in vivo, and ex vivo models, points to the toxic Aβ oligomers (AβO)s rather than amyloid plaques as key players in AD pathogenesis [79,80,81].”

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Authors
Fontana, I. C., Zimmer, A. R., Rocha, A. S., Gosmann, G., Souza, D. O., Lourenco, M. V., Ferreira, S. T., & Zimmer, E. R.
Affiliations
  • Universidade Federal do Rio Grande do Sul (BR)
  • Graduate Program in Biological Sciences: Biochemistry UFRGS Porto Alegre Brazil
  • Universidade Federal do Rio de Janeiro (BR)
Corresponding author
Zimmer, Eduardo R.
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2020-05-18
Volume
155
Issue
4
Pages
348-369
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W3017075749
Cited by
115
References
227
Citations by year
2026: 19 · 2025: 25 · 2024: 17 · 2023: 17 · 2022: 14 · 2021: 17 · 2020: 4
FWCI
1.66
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (202.817/2016)
  • Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul (ARD/PPP ‐ 16/2551‐0000175‐8, MS/CNPq/SESRS–PPSUS ‐ 30786.434.24734.23112017, PRONEX, FAPERGS/CNPq ‐ 16/2551‐0000475‐7)
  • Alzheimer's Association (AARG‐D‐615741)
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (309759/2017‐0, 311487/2019‐0, 420661/2016‐6, 451195/2017‐5, 460172/2014‐0, INCT ‐ 465346/2014‐6, INCT ‐ 465671/2014‐4)
  • Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (88881.141186/2017‐01)
  • International Society for Neurochemistry (ISN‐CAEN 1B)
  • Institute for Translational Neuroscience
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
amyloid-beta oligomers, Alzheimer's disease, amyloid-beta aggregation, synaptotoxicity, neurotoxicity, cell model, neurons, glial cells, amyloid plaques
MeSH terms
Alzheimer Disease, Amyloid, Animals, Brain, Cells, Cultured, Humans, Neurons, Amyloid beta-Peptides, Neural Stem Cells, Protein Aggregation, Pathological

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