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Mechanism of Oxidative Stress in Neurodegeneration

Gandhi, S; Abramov, AY; (2012) Mechanism of Oxidative Stress in Neurodegeneration. Oxidative Medicine and Cellular Longevity , 2012 , Article 428010. 10.1155/2012/428010. Green open access

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Abstract

Biological tissues require oxygen to meet their energetic demands. However, the consumption of oxygen also results in the generation of free radicals that may have damaging effects on cells. The brain is particularly vulnerable to the effects of reactive oxygen species due to its high demand for oxygen, and its abundance of highly peroxidisable substrates. Oxidative stress is caused by an imbalance in the redox state of the cell, either by overproduction of reactive oxygen species, or by dysfunction of the antioxidant systems. Oxidative stress has been detected in a range of neurodegenerative disease, and emerging evidence from in vitro and in vivo disease models suggests that oxidative stress may play a role in disease pathogenesis. However, the promise of antioxidants as novel therapies for neurodegenerative diseases has not been borne out in clinical studies. In this review, we critically assess the hypothesis that oxidative stress is a crucial player in common neurodegenerative disease and discuss the source of free radicals in such diseases. Furthermore, we examine the issues surrounding the failure to translate this hypothesis into an effective clinical treatment.

Type: Article
Title: Mechanism of Oxidative Stress in Neurodegeneration
Open access status: An open access version is available from UCL Discovery
DOI: 10.1155/2012/428010
Publisher version: http://dx.doi.org/10.1155/2012/428010
Language: English
Additional information: © 2012 S. Gandhi and A. Y. Abramov. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Keywords: Science & Technology, Life Sciences & Biomedicine, Cell Biology, AMYLOID-BETA PEPTIDE, CYTOSOLIC PHOSPHOLIPASE A(2), NADPH OXIDASE, ALZHEIMERS-DISEASE, PARKINSONS-DISEASE, CELL-DEATH, COMPLEX-I, MITOCHONDRIAL DYSFUNCTION, UNCOUPLING PROTEIN-2, DOPAMINERGIC-NEURONS
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/10043727
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