The physiological production of reactive oxygen, nitrogen and sulfur species is necessary to maintain correct intra- and intercellular signaling in any living tissue. These reactive species are essential for the regulated performance of cellular functions. In fact, oxidative eustress is key for the maintenance of cell morphology, differentiation, proliferation and cell death, among other functions. Changes in the production of different reactive species and alterations in the regulation of different redox related enzymes can lead to oxidative distress, causing major cellular changes that are closely connected to the onset and progression of neurodegenerative pathologies. The identification of affected biochemical pathways related to redox regulation in different brain areas has shed light on the origin of neurodegeneration in the central nervous system. There is increasing evidence suggesting that redox changes occur in the early stages of neurodegenerative diseases such as Amyotrophic lateral sclerosis, Alzheimer disease, Huntington disease and Parkinson´s disease. However, the brain areas affected by these pathologies are different and the pathophysiological characteristics they display are distinct from one another.
Current research in the field of neurodegenerative diseases is throwing light on the nature of the molecular changes that occur before the appearance of symptoms and that ultimately lead to cellular changes, neuronal loss and histological alterations. Some of these molecular modifications are linked to redox signaling and thus, redox regulation of different cellular functions. Our current aim is to elucidate in detail how redox active molecules and proteins, as well as redox-regulated circuits are affected in different neurodegenerative diseases. This will allow us, not only to understand the nature of these pathologies and the redox link that unites them, but also to describe, which events may be targets for new and innovative therapeutic strategies that could be applied to prevent and palliate the symptoms caused by these pathologies.
To this day, the causes that give rise to the hallmarks and symptoms of many neurodegenerative pathologies remain elusive. Therefore, we are particularly interested in original articles focused on alterations of redox-active molecules and/or redox-regulated cellular pathways, mainly in the early stages of neurodegenerative diseases. We also welcome the submission of clinical studies demonstrating changes in the levels of redox related molecules and altered redox states in different stages of neurodegenerative diseases. It is our aim to increase the knowledge related to the biochemical changes linked to redox homeostasis that give rise to neurodegeneration. Thus, review articles discussing the current state of the art are also welcome. This collection will allow us to better comprehend the nature of these pathologies and find new and innovative therapeutic targets to counter them in the future.
The physiological production of reactive oxygen, nitrogen and sulfur species is necessary to maintain correct intra- and intercellular signaling in any living tissue. These reactive species are essential for the regulated performance of cellular functions. In fact, oxidative eustress is key for the maintenance of cell morphology, differentiation, proliferation and cell death, among other functions. Changes in the production of different reactive species and alterations in the regulation of different redox related enzymes can lead to oxidative distress, causing major cellular changes that are closely connected to the onset and progression of neurodegenerative pathologies. The identification of affected biochemical pathways related to redox regulation in different brain areas has shed light on the origin of neurodegeneration in the central nervous system. There is increasing evidence suggesting that redox changes occur in the early stages of neurodegenerative diseases such as Amyotrophic lateral sclerosis, Alzheimer disease, Huntington disease and Parkinson´s disease. However, the brain areas affected by these pathologies are different and the pathophysiological characteristics they display are distinct from one another.
Current research in the field of neurodegenerative diseases is throwing light on the nature of the molecular changes that occur before the appearance of symptoms and that ultimately lead to cellular changes, neuronal loss and histological alterations. Some of these molecular modifications are linked to redox signaling and thus, redox regulation of different cellular functions. Our current aim is to elucidate in detail how redox active molecules and proteins, as well as redox-regulated circuits are affected in different neurodegenerative diseases. This will allow us, not only to understand the nature of these pathologies and the redox link that unites them, but also to describe, which events may be targets for new and innovative therapeutic strategies that could be applied to prevent and palliate the symptoms caused by these pathologies.
To this day, the causes that give rise to the hallmarks and symptoms of many neurodegenerative pathologies remain elusive. Therefore, we are particularly interested in original articles focused on alterations of redox-active molecules and/or redox-regulated cellular pathways, mainly in the early stages of neurodegenerative diseases. We also welcome the submission of clinical studies demonstrating changes in the levels of redox related molecules and altered redox states in different stages of neurodegenerative diseases. It is our aim to increase the knowledge related to the biochemical changes linked to redox homeostasis that give rise to neurodegeneration. Thus, review articles discussing the current state of the art are also welcome. This collection will allow us to better comprehend the nature of these pathologies and find new and innovative therapeutic targets to counter them in the future.
