Amyloid-β oligomers in cellular models of Alzheimer’s disease
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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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].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [5]
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].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [5]
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].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [5]
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].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [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.
- ORCID
- 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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