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Inicio Neurología (English Edition) Oxidative stress in neurological disease: Is it the cause, consequence, or trigg...
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Vol. 31. Issue 6.
Pages 420-421 (July - August 2016)
Vol. 31. Issue 6.
Pages 420-421 (July - August 2016)
Letter to the Editor
DOI: 10.1016/j.nrleng.2016.06.003
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Oxidative stress in neurological disease: Is it the cause, consequence, or trigger of a chronic progressive form?
Estrés oxidativo en la enfermedad neurológica. ¿Es causa, consecuencia o induce una forma crónica progresiva?
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J.A. Serraa, E.R. Marschoffb, R.O. Domínguezc,
Corresponding author
dominguezraulo@yahoo.com.ar

Corresponding author.
a Doctor en Ciencias Químicas, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Instituto de Bioquímica y Medicina Molecular (IBIMOL-Facultad de Farmacia y Bioquímica de la Universidad de Buenos Aires), Argentina
b Doctor en Ciencias Biológicas, Facultad de Ciencias Exactas y Naturales de la Universidad de Buenos Aires, Argentina
c Doctor en Medicina, Profesor de Neurología, Departamento de Neurología del Hospital Sirio Libanés, Facultad de Medicina de la Universidad de Buenos Aires, Argentina
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Dear Editor:

We have read with great interest the article published in October 2014 titled ‘Oxidative stress in neurological diseases: cause or effect?’1 and, as we find ourselves in agreement with the concepts expressed by the authors, we would like to present here some pertinent items of interest which have been published in the scientific literature over the past 25 years. Systemic oxidative stress (OS) is basically an imbalance between the production of such oxidants as reactive oxygen species (ROS) and reactive nitrogen species (RNS), and the capacity to neutralise their detrimental effects through both exogenous (diet and medication) and endogenous antioxidants.2 The affected neural areas present different morphological and metabolic changes; likely, the individual characteristics of each group of neurons is what determines their strengths or weaknesses in the face of OS. Systemic OS, which can be measured in blood analyses, is increased in such entities as Alzheimer disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), chronic vascular encephalopathy (CVE), epilepsy, and Friedreich ataxia, among others.3–8 In the same way, such clinical diseases as diabetes mellitus (DM), cancer, atherosclerosis, and chronic inflammation of the liver, kidney, and lung have been associated with systemic OS. Since the 1990s, a number of studies have described an association between ROS/antioxidants and AD, PD, and CVE. In addition, it has been shown that systemic OS is not identical in each of these entities. One of the most interesting findings was that OS was significantly lower in patients with both AD and type 2 DM than in patients with either AD or type 2 DM alone. The same was true for cognitive impairment.9–12 This may be due to hyperinsulinaemia and/or to glycaemia-lowering drugs.12 In conclusion, systemic OS must be located between the 2 extremes of cause or effect as it may be a factor contributing to pathological metabolic changes in a number of diseases. Reaching a balance between ROS and antioxidants may possibly diminish the risk of progression of these entities. Therefore, an emphasis should be made on the development of pharmacological studies aimed at minimising systemic OS.

Conflicts of interest

The authors declare that they have no conflicts of interest involving specific companies. All of the authors are familiar with the content of the manuscript and have given their permission to publish it. This manuscript has received no funding of any kind.

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Please cite this article as: Serra JA, Marschoff ER, Domínguez RO. Estrés oxidativo en la enfermedad neurológica. ¿Es causa, consecuencia o induce una forma crónica progresiva? Neurología. 2016;31:420–421.

Copyright © 2014. Sociedad Española de Neurología
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