Anti-TLR2 antibody triggers oxidative phosphorylation in microglia and increases phagocytosis of β-amyloid

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Date
2018-08-31
Authors
Rubio-Araiz, Ana
Finucane, Orla M.
Keogh, Samuel
Lynch, Marina A.
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Publisher
BioMed Central Ltd.
Published Version
10.1186/s12974-018-1281-7
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Abstract
Microglia are multifunctional cells that are primarily neuroprotective and a deficit in their functional integrity is likely to be a contributory factor in the deteriorating neuronal function that occurs with age and neurodegeneration. One aspect of microglial dysfunction is reduced phagocytosis, and this is believed to contribute to the accumulation of amyloid-β (Aβ) in Alzheimer’s disease (AD). Therefore, improving phagocytosis should be beneficial in limiting the amyloidosis that characterises AD.
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Keywords
Toll-like receptor 2 (TLR2) , Amyloid-β (Aβ) , Microglia , Neuroinflammation , Glycolysis , Oxidative metabolism , Phagocytosis
Citation
Rubio-Araiz, A., Finucane, O.M., Keogh, S. and Lynch, M.A., 2018. Anti-TLR2 antibody triggers oxidative phosphorylation in microglia and increases phagocytosis of β-amyloid. Journal of neuroinflammation, 15(1), 247, (13 pp.). DOI:10.1186/s12974-018-1281-7
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https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-018-1281-7
URI
https://hdl.handle.net/10468/8902
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Anatomy and Neuroscience - Journal Articles
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© The Author(s). 2018, Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.