The redox system is a ubiquitous homeostatic system, whose primary purpose is to allow an organism to react to environmental challenges (internal or external), through the activation of adaptive mechanisms, aimed at survival, based on redox reactions. In its simplest mode of operation, the redox system provides for the reversible or irreversible oxidation of a molecular target (e.g., a transcription factor or a bacterial component) by oxidizing species (e.g. hydrogen peroxide or hydroxyl radical) in order to modulate a function (activation of a signaling pathway or neutralization of a potentially toxic agent) and the consequent return to the basal condition through the intervention of reducing species, capable to return, when possible, the electron to the molecular target and, possibly, to the oxidizing species (if in excess). When the adaptive response of the redox system is successful, a condition of “oxidative eu-stress” occurs; if, on the other hand, the adaptive response fails, we must label that as “oxidative di-stress”, associated with premature aging and numerous chronic and degenerative diseases, including neurodegenerative disorders (i.e., Parkinson’s disease, Alzheimer’s diseases, Lateral Amyotrophic and Multiple Sclerosis).
The biological complexity of the nervous system translates into a marked complexity of the redox system at the molecular level, within its heterogeneous components both cellular, vascular and extracellular ones. For example, mitochondria dysfunction, both metabolic and related to dynamic changes of morphology and connectivity (fusion, fission), is linked with sustained oxidative di-stress in neurodegenerative disorders. However, the exact molecular pathogenesis of neurodegeneration related to the disturbance of redox balance remains unclear. Furthermore, oxidative di-stress can be associated with a condition of chronic silent inflammation, but can proceed independently of it, while inflammation is always associated to oxidative distress. The development of cell-based therapies for regenerative medicine in the central nervous system disorders, represents an exciting challenge. Indeed, stem cells (somatic stem cells or iPSCs) may enhance endogenous neuroplasticity, through their paracrine effects, and protect existing healthy neurons and glial cells from further damage, as inflammation, while differentiated cells may repair the injured neuronal tissue, by replacing the damaged or lost cells.
As such, we welcome original research, reviews and perspective articles (among others) that address the following Themes, with the focus on addressing these aspects of redox homeostasis in neurodegenerative diseases:
(i) understanding the physiological role of the redox system in the nervous system, by compartment, by cell type, in different evolutionary stages, in basal conditions and after stimulus
(ii) identifying the mechanisms through which the redox system modulates signaling, the reactive phenomena of the glia and neurogenesis
(iii) defining the impact of inflammation, epigenetics and microbiome on the redox system
(iv) developing suitable study models or use those currently available in a targeted manner
(v) developing suitable methodologies for the study of redox phenomena (interactomics, redoxomics, metabolomics, functional imaging, in vivo redox imaging).
Only on this basis could we tackle the study of neurodegenerative diseases in view of sustainable solutions, where regenerative medicine, from an integrated and multidisciplinary perspective, is a candidate to play a crucial role. We solicit and encourage contributions on these issues that we believe crucial in the understanding and control of neurodegenerative diseases.
The redox system is a ubiquitous homeostatic system, whose primary purpose is to allow an organism to react to environmental challenges (internal or external), through the activation of adaptive mechanisms, aimed at survival, based on redox reactions. In its simplest mode of operation, the redox system provides for the reversible or irreversible oxidation of a molecular target (e.g., a transcription factor or a bacterial component) by oxidizing species (e.g. hydrogen peroxide or hydroxyl radical) in order to modulate a function (activation of a signaling pathway or neutralization of a potentially toxic agent) and the consequent return to the basal condition through the intervention of reducing species, capable to return, when possible, the electron to the molecular target and, possibly, to the oxidizing species (if in excess). When the adaptive response of the redox system is successful, a condition of “oxidative eu-stress” occurs; if, on the other hand, the adaptive response fails, we must label that as “oxidative di-stress”, associated with premature aging and numerous chronic and degenerative diseases, including neurodegenerative disorders (i.e., Parkinson’s disease, Alzheimer’s diseases, Lateral Amyotrophic and Multiple Sclerosis).
The biological complexity of the nervous system translates into a marked complexity of the redox system at the molecular level, within its heterogeneous components both cellular, vascular and extracellular ones. For example, mitochondria dysfunction, both metabolic and related to dynamic changes of morphology and connectivity (fusion, fission), is linked with sustained oxidative di-stress in neurodegenerative disorders. However, the exact molecular pathogenesis of neurodegeneration related to the disturbance of redox balance remains unclear. Furthermore, oxidative di-stress can be associated with a condition of chronic silent inflammation, but can proceed independently of it, while inflammation is always associated to oxidative distress. The development of cell-based therapies for regenerative medicine in the central nervous system disorders, represents an exciting challenge. Indeed, stem cells (somatic stem cells or iPSCs) may enhance endogenous neuroplasticity, through their paracrine effects, and protect existing healthy neurons and glial cells from further damage, as inflammation, while differentiated cells may repair the injured neuronal tissue, by replacing the damaged or lost cells.
As such, we welcome original research, reviews and perspective articles (among others) that address the following Themes, with the focus on addressing these aspects of redox homeostasis in neurodegenerative diseases:
(i) understanding the physiological role of the redox system in the nervous system, by compartment, by cell type, in different evolutionary stages, in basal conditions and after stimulus
(ii) identifying the mechanisms through which the redox system modulates signaling, the reactive phenomena of the glia and neurogenesis
(iii) defining the impact of inflammation, epigenetics and microbiome on the redox system
(iv) developing suitable study models or use those currently available in a targeted manner
(v) developing suitable methodologies for the study of redox phenomena (interactomics, redoxomics, metabolomics, functional imaging, in vivo redox imaging).
Only on this basis could we tackle the study of neurodegenerative diseases in view of sustainable solutions, where regenerative medicine, from an integrated and multidisciplinary perspective, is a candidate to play a crucial role. We solicit and encourage contributions on these issues that we believe crucial in the understanding and control of neurodegenerative diseases.
