Oxidative stress occurs due to the imbalance between antioxidants and free radicals in the body, which can further result in tissue and cell injury. In the aging process, oxidative stress has a noteworthy contribution. The mitochondrial respiratory chain and enzymatic activities are the endogenous sources of reactive oxygen species. Various oxidizing chemicals, ionizing radiation, and ultraviolet light are known as the inducing stressors of exogenous reactive oxygen species. Reactive oxygen species play a role as a vital second messenger in cell signaling pathways at lower concentrations. Nonetheless, long-term exposure and at high concentrations, reactive oxygen species can result in injury of various cellular macromolecules, including lipids, proteins, and DNA, which can further lead to apoptotic and necrotic cell death.
A lower level of antioxidant activity has been detected in the brain as compared to other tissues. Indeed, cells have the capacity to counteract oxidant injury via controlling their homeostatic balance under normal conditions. Nevertheless, the ability of cells to preserve the redox balance reduces during the advancement of age-associated neurodegenerative disorders, which can further result in neuronal injury, mitochondrial dysfunction, and buildup of free radicals. Oxidative stress level elevates during the aging process. Moreover, oxidative stress is responsible for the advancement of multiple neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, etc. Findings from genetic research have suggested that various proteins including superoxide dismutase, amyloid-β, and α-synuclein play a substantial role in pathogenesis of amyotrophic lateral sclerosis, Alzheimer's, and Parkinson's diseases, respectively. Furthermore, these proteins are the key constituents of the neuronal deposits linked with these neurodegenerative disorders. These proteins have also been reported to interact with redox-active metal ions that further mediate free radicals generation. Aberrant interactions amid proteins can lead to abnormal extracellular and intracellular deposition of self-aggregating misfolded proteins with the generation of higher-order insoluble fibrils are the commonly observed pathological hallmarks of several neurodegenerative diseases.
In this special thematic issue, we welcome neuroscientists to contribute their articles exploring the linkage of oxidative stress and neurodegenerative disorders. Furthermore, this issue aimed to collect articles highlighting the recent growth in the management of neurodegenerative insults.
Dr. Ghulam Md Ashraf
Manuscripts should be submitted via our online editorial system at https://imr.propub.com by registering and logging in to this website. Once you are registered, click here to start your submission. Manuscripts can be submitted now or up until the deadline. All papers will go through peer-review process. Accepted papers will be published in the journal (as soon as accepted) and meanwhile listed together on the special issue website. Research articles, reviews as well as short communications are preferred. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office to announce on this website.
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