Abstract
Background: Neurodegeneration is a condition in which progressive loss of function and structure of neurons occurs. Several lines of evidence suggest that oxidative stress has a central role in neurodegenerative diseases.
Objective: The aim was to survey molecular mechanisms underlying the involvement of oxidative stress in developing different neurodegenerative diseases.
Methods: Original and review articles were retrieved through a PubMed and Google scholar search (from 1989 to 2015) using the following key words: “oxidative stress”, “nerve degeneration” and “neurodegenerative diseases”.
Results: A comprehensive analysis of the obtained articles confirmed strong involvement of oxidative stress in the pathophysiology of neurodegenerative diseases through a variety of mechanisms including induction of oxidation of nucleic acids, proteins and lipids, formation of advanced glycation end products, mitochondrial dysfunction, glial cell activation, amyloid β deposition and plaque formation, apoptosis, cytokine production and inflammatory responses, and proteasome dysfunction.
Conclusion: Regarding the pivotal role of oxidative stress in neurodegeneration, modulation of free radical production or alleviating their harmful effects can be considered as a potential therapeutic strategy for preventing and controlling neurodegenerative diseases. Accordingly; boosting endogenous antioxidant capacity besides providing exogenous sources of antioxidants merits future research in order to discover new therapeutic agents.
Keywords: Oxidative stress, nerve degeneration, neurodegenerative disease, Alzheimer's disease, parkinson's disease, huntington's disease.
CNS & Neurological Disorders - Drug Targets
Title:The Underlying Role of Oxidative Stress in Neurodegeneration: A Mechanistic Review
Volume: 17 Issue: 3
Author(s): Habib Yaribeygi, Yunes Panahi*, Behjat Javadi and Amirhossein Sahebkar*
Affiliation:
- Pharmacotherapy Department, School of Pharmacy, Baqiyatallah University of Medical Sciences, Tehran,Iran
- Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad,Iran
Keywords: Oxidative stress, nerve degeneration, neurodegenerative disease, Alzheimer's disease, parkinson's disease, huntington's disease.
Abstract: Background: Neurodegeneration is a condition in which progressive loss of function and structure of neurons occurs. Several lines of evidence suggest that oxidative stress has a central role in neurodegenerative diseases.
Objective: The aim was to survey molecular mechanisms underlying the involvement of oxidative stress in developing different neurodegenerative diseases.
Methods: Original and review articles were retrieved through a PubMed and Google scholar search (from 1989 to 2015) using the following key words: “oxidative stress”, “nerve degeneration” and “neurodegenerative diseases”.
Results: A comprehensive analysis of the obtained articles confirmed strong involvement of oxidative stress in the pathophysiology of neurodegenerative diseases through a variety of mechanisms including induction of oxidation of nucleic acids, proteins and lipids, formation of advanced glycation end products, mitochondrial dysfunction, glial cell activation, amyloid β deposition and plaque formation, apoptosis, cytokine production and inflammatory responses, and proteasome dysfunction.
Conclusion: Regarding the pivotal role of oxidative stress in neurodegeneration, modulation of free radical production or alleviating their harmful effects can be considered as a potential therapeutic strategy for preventing and controlling neurodegenerative diseases. Accordingly; boosting endogenous antioxidant capacity besides providing exogenous sources of antioxidants merits future research in order to discover new therapeutic agents.
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Cite this article as:
Yaribeygi Habib , Panahi Yunes *, Javadi Behjat and Sahebkar Amirhossein *, The Underlying Role of Oxidative Stress in Neurodegeneration: A Mechanistic Review, CNS & Neurological Disorders - Drug Targets 2018; 17 (3) . https://dx.doi.org/10.2174/1871527317666180425122557
DOI https://dx.doi.org/10.2174/1871527317666180425122557 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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