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

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

Igor C Fontana  1   2 , Aline R Zimmer  1 , Andreia S Rocha  2 , Grace Gosmann  1 , Diogo O Souza  2   3 , Mychael V Lourenco  4 , Sergio T Ferreira  4   5 , Eduardo R Zimmer  2   6   7
Affiliations
Free article
Review

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

Igor C Fontana et al. J Neurochem. 2020 Nov.
Free article

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.

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References

REFERENCES

    1. Abbasi, J. (2018). Promising results in 18-month analysis of Alzheimer drug candidate. JAMA, 320, 965. https://doi.org/10.1001/jama.2018.13027
    1. Abramov, A. Y., Canevari, L., & Duchen, M. R. (2004). Beta-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase. Journal of Neuroscience, 24, 565-575. https://doi.org/10.1523/JNEUROSCI.4042-03.2004
    1. Abramovitch-Dahan, C., Asraf, H., Bogdanovic, M., Sekler, I., Bush, A. I., & Hershfinkel, M. (2016). Amyloid beta attenuates metabotropic zinc sensing receptor, mZnR/GPR39, dependent Ca2+, ERK1/2 and Clusterin signaling in neurons. Journal of Neurochemistry, 139, 221-233.
    1. Agholme, L., Lindstrom, T., Kagedal, K., Marcusson, J., & Hallbeck, M. (2010). An in vitro model for neuroscience: Differentiation of SH-SY5Y cells into cells with morphological and biochemical characteristics of mature neurons. Journal of Alzheimer's Disease, 20, 1069-1082. https://doi.org/10.3233/JAD-2010-091363
    1. Ahmed, M., Davis, J., Aucoin, D., Sato, T., Ahuja, S., Aimoto, S., … Smith, S. O. (2010). Structural conversion of neurotoxic amyloid-beta(1-42) oligomers to fibrils. Nature Structural & Molecular Biology, 17, 561-567.

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