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      The Role of Oxidative Stress in Neurodegenerative Diseases

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          Abstract

          Oxidative stress is induced by an imbalanced redox states, involving either excessive generation of reactive oxygen species (ROS) or dysfunction of the antioxidant system. The brain is one of organs especially vulnerable to the effects of ROS because of its high oxygen demand and its abundance of peroxidation-susceptible lipid cells. Previous studies have demonstrated that oxidative stress plays a central role in a common pathophysiology of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Antioxidant therapy has been suggested for the prevention and treatment of neurodegenerative diseases, although the results with regard to their efficacy of treating neurodegenerative disease have been inconsistent. In this review, we will discuss the role of oxidative stress in the pathophysiology of neurodegenerative diseases and in vivo measurement of an index of damage by oxidative stress. Moreover, the present knowledge on antioxidant in the treatment of neurodegenerative diseases and future directions will be outlined.

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          Glutathione peroxidases.

          Regina Brigelius-Flohé, Matilde Maiorino (2013)
          With increasing evidence that hydroperoxides are not only toxic but rather exert essential physiological functions, also hydroperoxide removing enzymes have to be re-viewed. In mammals, the peroxidases inter alia comprise the 8 glutathione peroxidases (GPx1-GPx8) so far identified. Since GPxs have recently been reviewed under various aspects, we here focus on novel findings considering their diverse physiological roles exceeding an antioxidant activity. GPxs are involved in balancing the H2O2 homeostasis in signalling cascades, e.g. in the insulin signalling pathway by GPx1; GPx2 plays a dual role in carcinogenesis depending on the mode of initiation and cancer stage; GPx3 is membrane associated possibly explaining a peroxidatic function despite low plasma concentrations of GSH; GPx4 has novel roles in the regulation of apoptosis and, together with GPx5, in male fertility. Functions of GPx6 are still unknown, and the proposed involvement of GPx7 and GPx8 in protein folding awaits elucidation. Collectively, selenium-containing GPxs (GPx1-4 and 6) as well as their non-selenium congeners (GPx5, 7 and 8) became key players in important biological contexts far beyond the detoxification of hydroperoxides. This article is part of a Special Issue entitled Cellular functions of glutathione. Copyright © 2012 Elsevier B.V. All rights reserved.
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            Vitamin E and donepezil for the treatment of mild cognitive impairment.

            Ronald Petersen, Ronald Thomas, Michael Grundman … (2005)
            Mild cognitive impairment is a transitional state between the cognitive changes of normal aging and early Alzheimer's disease. In a double-blind study, we evaluated subjects with the amnestic subtype of mild cognitive impairment. Subjects were randomly assigned to receive 2000 IU of vitamin E daily, 10 mg of donepezil daily, or placebo for three years. The primary outcome was clinically possible or probable Alzheimer's disease; secondary outcomes were cognition and function. A total of 769 subjects were enrolled, and possible or probable Alzheimer's disease developed in 212. The overall rate of progression from mild cognitive impairment to Alzheimer's disease was 16 percent per year. As compared with the placebo group, there were no significant differences in the probability of progression to Alzheimer's disease in the vitamin E group (hazard ratio, 1.02; 95 percent confidence interval, 0.74 to 1.41; P=0.91) or the donepezil group (hazard ratio, 0.80; 95 percent confidence interval, 0.57 to 1.13; P=0.42) during the three years of treatment. Prespecified analyses of the treatment effects at 6-month intervals showed that as compared with the placebo group, the donepezil group had a reduced likelihood of progression to Alzheimer's disease during the first 12 months of the study (P=0.04), a finding supported by the secondary outcome measures. Among carriers of one or more apolipoprotein E epsilon4 alleles, the benefit of donepezil was evident throughout the three-year follow-up. There were no significant differences in the rate of progression to Alzheimer's disease between the vitamin E and placebo groups at any point, either among all patients or among apolipoprotein E epsilon4 carriers. Vitamin E had no benefit in patients with mild cognitive impairment. Although donepezil therapy was associated with a lower rate of progression to Alzheimer's disease during the first 12 months of treatment, the rate of progression to Alzheimer's disease after three years was not lower among patients treated with donepezil than among those given placebo. Copyright 2005 Massachusetts Medical Society.
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              Antioxidant responses and cellular adjustments to oxidative stress

              Cristina Espinosa-Díez, Verónica Miguel, Daniela Mennerich … (2015)
              Redox biological reactions are now accepted to bear the Janus faceted feature of promoting both physiological signaling responses and pathophysiological cues. Endogenous antioxidant molecules participate in both scenarios. This review focuses on the role of crucial cellular nucleophiles, such as glutathione, and their capacity to interact with oxidants and to establish networks with other critical enzymes such as peroxiredoxins. We discuss the importance of the Nrf2-Keap1 pathway as an example of a transcriptional antioxidant response and we summarize transcriptional routes related to redox activation. As examples of pathophysiological cellular and tissular settings where antioxidant responses are major players we highlight endoplasmic reticulum stress and ischemia reperfusion. Topologically confined redox-mediated post-translational modifications of thiols are considered important molecular mechanisms mediating many antioxidant responses, whereas redox-sensitive microRNAs have emerged as key players in the posttranscriptional regulation of redox-mediated gene expression. Understanding such mechanisms may provide the basis for antioxidant-based therapeutic interventions in redox-related diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Exp Neurobiol
                Journal ID (iso-abbrev): Exp Neurobiol
                Journal ID (publisher-id): EN
                Title: Experimental Neurobiology
                Publisher: The Korean Society for Brain and Neural Science
                ISSN (Print): 1226-2560
                ISSN (Electronic): 2093-8144
                Publication date (Print): December 2015
                Publication date (Electronic): 12 October 2015
                Volume: 24
                Issue: 4
                Pages: 325-340
                Affiliations
                [1 ]Ewha Brain Institute, Ewha Womans University, Seoul 03760, Korea.
                [2 ]Department of Neurology, Ewha Womans University Mokdong Hospital, Ewha Womans University School of Medicine, Seoul 03760, Korea.
                [3 ]Department of Brain and Cognitive Sciences, Ewha Womans University, Seoul 03760, Korea.
                [4 ]College of Pharmacy, Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul 03760, Korea.
                Author notes
                To whom correspondence should be addressed. TEL: 82-2-3277-2466, FAX: 82-2-3277-6562, sujungjyoon@ 123456ewha.ac.kr
                Article
                DOI: 10.5607/en.2015.24.4.325
                PMC ID: 4688332
                PubMed ID: 26713080
                SO-VID: 671705e8-7961-4ab9-9aa5-475cc990d3ba
                Copyright © Copyright © Experimental Neurobiology 2015.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 20 August 2015
                Date revision received : 14 September 2015
                Date accepted : 14 September 2015
                Funding
                Funded by: MSIP, CrossRef http://dx.doi.org/10.13039/501100003621;
                Award ID: B0132-15-1001
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Neurosciences
                Keywords: oxidative stress,reactive oxygen species,neurodegenerative disease,alzheimer's disease,parkinson's disease,antioxidant
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: oxidative stress, reactive oxygen species, neurodegenerative disease, alzheimer's disease, parkinson's disease, antioxidant

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