About this Research Topic
Antioxidants have been considered as attractive potential therapeutic agents to prevent or halt disease progression but the clinical efficacy of antioxidant treatment strategies is still marginal. Improvement of antioxidant therapy effectiveness might involve adjustment of preclinical to clinical settings and development of new efficient delivery methods and will require a more in-depth knowledge of cellular redox-signaling mechanisms. Promising novel redox-based therapeutic strategies are gaining relevance to combat oxidative stress associated with neurodegenerative diseases. These include boosting the endogenous antioxidant machinery through activation of the antioxidant master regulator Nrf2 (nuclear factor erythroid 2-related factor 2) or modulation of ROS production by NOX (nicotinamide adenine dinucleotide phosphate (NADPH) oxidase) inhibitors.
Redox regulation of key cellular functions is currently recognized as an important cellular signaling mechanism and events such as post-translational modifications (e.g. S_glutathionylation, S_nitrosylation, glycosylation, etc) play important roles in redox signal transduction and might be instrumental to uncover pathological mechanisms and identify novel therapeutic targets in neurodegenerative diseases.
This Research Topic focuses on redox signaling mechanisms and aims to provide novel insights into the role of redox-signaling, with particular emphasis on redox regulation involving post-translational modifications, in the pathophysiology of neurodegenerative diseases. Moreover, it aims to present an overview of the potential of antioxidants as therapeutics for CNS disorders with a special focus on emerging novel therapeutic redox-based strategies.
We are particularly interested in studies: -addressing new redox-based molecular mechanisms contributing to neurodegenerative diseases; -exploring the role of naturally occurring compounds, standard medications, and nutraceuticals with antioxidant properties in modulating redox-signaling pathways and limiting and/or preventing oxidative damage associated with these disorders; -addressing mechanistically the role of post-translational modifications in the pathophysiology of neurodegenerative disorders.
We invite investigators to contribute original research articles, brief research reports, and methods as well as review or mini-review articles that contribute to deepening our understanding of how oxidative stress is involved in neurodegenerative processes, and to the identification of molecular mechanisms on how reactive species trigger and contribute to the progression of neurodegenerative diseases. Lastly, we will accept manuscripts that describe the development of novel therapeutic strategies aimed to restore the delicate redox balance and halt neurodegeneration.
Potential topics to be addressed include, but are not limited to:
· Mechanisms of redox regulation in neurophysiology and neuropathology
· Novel cellular and molecular mechanisms linking thiol-based redox homeostasis disturbance to neurodegeneration
· Molecular mechanisms and clinical significance of post-translational modifications with impact on cellular redox status and neuronal (dys)function and degeneration (e.g. S_Glutathionylation; S-Nitrosylation; Glycosylation, etc)
· Novel modulators of post-translational modifications of proteins during oxidative stress
· Novel compounds/therapeutic approaches aiming to prevent and/or limit oxidative damage in the context of neurodegenerative diseases
· Promising therapeutic approaches aiming to enhance endogenous antioxidant defense machinery to combat oxidative stress in the CNS
Keywords: Oxidative stress, Antioxidants, Neurodegenerative diseases, Post-translational modifications, Redox-signaling
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.