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Interaction of Oxidative Stress and Misfolded Proteins in the Mechanism of Neurodegeneration

Abramov, AY; Potapova, EV; Dremin, VV; Dunaev, AV; (2020) Interaction of Oxidative Stress and Misfolded Proteins in the Mechanism of Neurodegeneration. Life , 10 (7) , Article 101. 10.3390/life10070101. Green open access

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Abstract

Aggregation of the misfolded proteins β-amyloid, tau, huntingtin, and α-synuclein is one of the most important steps in the pathology underlying a wide spectrum of neurodegenerative disorders, including the two most common ones-Alzheimer's and Parkinson's disease. Activity and toxicity of these proteins depends on the stage and form of aggregates. Excessive production of free radicals, including reactive oxygen species which lead to oxidative stress, is proven to be involved in the mechanism of pathology in most of neurodegenerative disorders. Both reactive oxygen species and misfolded proteins play a physiological role in the brain, and only deregulation in redox state and aggregation of the proteins leads to pathology. Here, we review the role of misfolded proteins in the activation of ROS production from various sources in neurons and glia. We discuss if free radicals can influence structural changes of the key toxic intermediates and describe the putative mechanisms by which oxidative stress and oligomers may cause neuronal death.

Type: Article
Title: Interaction of Oxidative Stress and Misfolded Proteins in the Mechanism of Neurodegeneration
Location: Switzerland
Open access status: An open access version is available from UCL Discovery
DOI: 10.3390/life10070101
Publisher version: https://doi.org/10.3390/life10070101
Language: English
Additional information: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
Keywords: Mutant huntingtin protein, neurodegeneration, oxidative stress, reactive oxygen species, tau protein, α-synuclein, β-amyloid
UCL classification: UCL
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Movement Neurosciences
URI: https://discovery.ucl.ac.uk/id/eprint/10106002
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