Special Issue "Free Radicals and Antioxidants in Neuroinflammation"

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A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (28 February 2014)

Special Issue Editors

Guest Editor
Prof. Dr. Jack van Horssen

Department of Molecular Cell Biology and Immunology, VU University Medical Center Amsterdam, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
Website | E-Mail
Phone: 0031204448078
Fax: +31 204448081
Interests: immunohistochemistry; neuropathology; neuroinflammation; mitochondrial dysfunction; Nrf2; antioxidant enzymes; multiple sclerosis
Co-Guest Editor
Dr. Maarten E. Witte

Department of Molecular Cell Biology and Immunology, VU University Medical Center Amsterdam, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
E-Mail
Fax: +31 20 4448081
Interests: neuroinflammation; neurodegeneration; mitochondrial biology; energy metabolism; oxidative stress

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) are continuously produced in the central nervous system (CNS) by ROS-generating enzymes, such as NADPH oxidases, and by mitochondria. Importantly, ROS are efficiently detoxified by endogenous cytosolic and mitochondrial antioxidant enzymes in order to prevent oxidative injury to vulnerable CNS cells. However, in neuroinflammatory diseases, ROS production exceeds the antioxidant capacity. This results in irreversible oxidative damage to essential cellular structures, and eventually leads to neuronal loss. The aim of this special issue is to provide a comprehensive overview on the involvement of oxidative stress in neuroinflammatory conditions. Specific topics include:

1. Elucidation of the (sub)cellular origin of ROS during a neuroinflammatory attack and the molecular processes that are involved in this process.

2. Therapeutic potential of endogenous antioxidants in neuroinflammation, including transcriptional regulation of antioxidant enzymes, such as the Nrf2 and PGC-1α pathway.

Prof. Dr. Jack van Horssen
Dr. Maarten E. Witte
Guest Editor
s

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed Open Access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 300 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.

Keywords

  • neurodegenerative diseases (Parkinson, Alzheimer)
  • ROS-generating enzymes (NADPH oxidase, NOS)
  • neuroinflammation
  • Nrf2 and PCG-alpha pathway
  • exogenous antioxidants
  • mitochondrial antioxidants
  • microglia activation
  • meningeal inflammation
  • antioxidant therapy
  • oxidative stress

Published Papers (2 papers)

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Research

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Open AccessArticle Oxidative Stress Is Associated with Neuroinflammation in Animal Models of HIV-1 Tat Neurotoxicity
Antioxidants 2014, 3(2), 414-438; doi:10.3390/antiox3020414
Received: 12 March 2014 / Revised: 18 April 2014 / Accepted: 5 May 2014 / Published: 16 May 2014
Cited by 1 | PDF Full-text (1163 KB) | HTML Full-text | XML Full-text
Abstract
HIV-1 trans-acting protein Tat, an essential protein for viral replication, is a key mediator of neurotoxicity. If Tat oxidant injury and neurotoxicity have been described, consequent neuroinflammation is less understood. Rat caudate-putamens (CPs) were challenged with Tat, with or without prior rSV40-delivered
[...] Read more.
HIV-1 trans-acting protein Tat, an essential protein for viral replication, is a key mediator of neurotoxicity. If Tat oxidant injury and neurotoxicity have been described, consequent neuroinflammation is less understood. Rat caudate-putamens (CPs) were challenged with Tat, with or without prior rSV40-delivered superoxide dismutase or glutathione peroxidase. Tat injection caused oxidative stress. Administration of Tat in the CP induced an increase in numbers of Iba-1- and CD68-positive cells, as well as an infiltration of astrocytes. We also tested the effect of more protracted Tat exposure on neuroinflammation using an experimental model of chronic Tat exposure. SV(Tat): a recombinant SV40-derived gene transfer vector was inoculated into the rat CP, leading to chronic expression of Tat, oxidative stress, and ongoing apoptosis, mainly located in neurons. Intra-CP SV(Tat) injection induced an increase in microglia and astrocytes, suggesting that protracted Tat production increased neuroinflammation. SV(SOD1) or SV(GPx1) significantly reduced neuroinflammation following Tat administration into the CP. Thus, Tat-induced oxidative stress, CNS injury, neuron loss and inflammation may be mitigated by antioxidant gene delivery. Full article
(This article belongs to the Special Issue Free Radicals and Antioxidants in Neuroinflammation)

Review

Jump to: Research

Open AccessReview Oxidative Stress and the Use of Antioxidants in Stroke
Antioxidants 2014, 3(3), 472-501; doi:10.3390/antiox3030472
Received: 24 February 2014 / Revised: 8 May 2014 / Accepted: 14 May 2014 / Published: 3 July 2014
Cited by 5 | PDF Full-text (823 KB) | HTML Full-text | XML Full-text
Abstract
Transient or permanent interruption of cerebral blood flow by occlusion of a cerebral artery gives rise to an ischaemic stroke leading to irreversible damage or dysfunction to the cells within the affected tissue along with permanent or reversible neurological deficit. Extensive research has
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Transient or permanent interruption of cerebral blood flow by occlusion of a cerebral artery gives rise to an ischaemic stroke leading to irreversible damage or dysfunction to the cells within the affected tissue along with permanent or reversible neurological deficit. Extensive research has identified excitotoxicity, oxidative stress, inflammation and cell death as key contributory pathways underlying lesion progression. The cornerstone of treatment for acute ischaemic stroke remains reperfusion therapy with recombinant tissue plasminogen activator (rt-PA). The downstream sequelae of events resulting from spontaneous or pharmacological reperfusion lead to an imbalance in the production of harmful reactive oxygen species (ROS) over endogenous anti-oxidant protection strategies. As such, anti-oxidant therapy has long been investigated as a means to reduce the extent of injury resulting from ischaemic stroke with varying degrees of success. Here we discuss the production and source of these ROS and the various strategies employed to modulate levels. These strategies broadly attempt to inhibit ROS production or increase scavenging or degradation of ROS. While early clinical studies have failed to translate success from bench to bedside, the combination of anti-oxidants with existing thrombolytics or novel neuroprotectants may represent an avenue worthy of clinical investigation. Clearly, there is a pressing need to identify new therapeutic alternatives for the vast majority of patients who are not eligible to receive rt-PA for this debilitating and devastating disease. Full article
(This article belongs to the Special Issue Free Radicals and Antioxidants in Neuroinflammation)

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