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HAL Id: hal-02328689

https://hal.archives-ouvertes.fr/hal-02328689

Submitted on 23 Oct 2019

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Editorial Neurodegeneration, Neurogenesis, and

Oxidative Stress 2015

Renata Santos, Anne-Laure Bulteau, Cláudio Gomes

To cite this version:

Renata Santos, Anne-Laure Bulteau, Cláudio Gomes. Editorial Neurodegeneration, Neurogenesis,

and Oxidative Stress 2015. Oxidative Medicine and Cellular Longevity, Hindawi, 2016, 2016, pp.1-1.

�10.1155/2016/7632025�. �hal-02328689�

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Editorial

Neurodegeneration, Neurogenesis, and Oxidative Stress 2015

Renata Santos,

1

Anne-Laure Bulteau,

2

and Cláudio M. Gomes

3

1Development of the Nervous System, IBENS, Ecole Normale Sup´erieure, 46 rue d’Ulm, 75230 Paris Cedex 05, France 2Iprem University of Pau, 2 rue du Pr´esident Angot, 64000 Pau, France

3Faculdade de Ciˆencias, Universidade de Lisboa, Biosystems and Integrative Sciences Institute and

Department of Chemistry and Biochemistry, Universidade de Lisboa, Campo Grande, 1749-016 Lisboa, Portugal

Correspondence should be addressed to Renata Santos; rsantos@biologie.ens.fr Received 21 December 2015; Accepted 21 December 2015

Copyright © 2016 Renata Santos et al. 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.

Oxidative stress is implicated in the pathophysiology of a wide variety of neurodegenerative disorders and its role in neurogenesis is becoming increasingly acknowledged. This special issue includes 8 articles that emphasize the implica-tions of oxidative stress in neurodegeneration, neurotoxicity, and neurogenesis.

Several original and review articles discuss the role of oxidative stress in neurodegenerative disorders and upon brain injury. S. K. Singh et al. open the issue by presenting a comprehensive review on the pathology of Alzheimer’s disease (AD). Two other review articles focus on specific aspects implicated in AD. L. Zuo et al. discuss how oxidative stress is related to AD progression and to the formation of A𝛽 plaques and tau neurofibrillary tangles. In addition, the authors examine evidence of epigenetic regulation of A𝛽 plaque formation in AD neurons and discuss different potential therapeutic approaches. J. S. Cristov˜ao et al. concen-trate on the role of metal ions in AD and overview different proteins implicated in AD whose metal binding properties may underlie important biochemical and regulatory pro-cesses occurring in the brain during the pathophysiological process. Hyperphosphorylation and aggregation of tau in neurons not only are a central feature in AD but are present in other neurodegenerative diseases, termed tauopathies. S. M. A. Naini and N. Soussi-Yanicostas review the relationship between tau pathology and oxidative stress and present arguments in favor of the hypothesis that these are key components of a pathologic vicious circle in tauopathies. In a different direction, X. Hu et al. summarize recent litera-ture describing the contribution of oxidative stress to brain

damage after intracerebral hemorrhage. H. J. Olgu´ın et al. describe dopamine dysfunction as a consequence of oxidative stress and discuss its implication in disease conditions, such as in Parkinson’s disease. In an original article, A. Seguin et al. present interesting data on a drug screen performed using two different models of Friedreich’s ataxia, yeast and

Drosophila. In the original article by B. P. Carreira et al.,

the authors examine the role of nitric oxide in neurogenesis in adult hippocampus following seizures. They show that although nitric oxide is beneficial in the early stages of production of newborn neural cells, it is detrimental to the survival of newly differentiated neurons due to inflammation.

Acknowledgments

We would like to thank all the authors and reviewers that participated in this issue.

Renata Santos Anne-Laure Bulteau Cl´audio M. Gomes

Hindawi Publishing Corporation Oxidative Medicine and Cellular Longevity Volume 2016, Article ID 7632025, 1 page http://dx.doi.org/10.1155/2016/7632025

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