Neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, multiple sclerosis, and amyotrophic lateral sclerosis, including acute stroke and age-related chronic disorders are known to result from mutations in membrane potential and cellular homeostasis, part of complex cellular events leading to neurodegeneration and brain disorders.
Intracellular redox-modulatory disturbances caused by oxidative stress (OS) are directly mediated by neuronal pathophysiology, and by the inability of endogenous and exogenous antioxidant defense mechanisms to neutralize accumulating reactive oxygen/nitrogen (ROS/RNS, including nitro-oxidative pathways) species. A potential strategy to regulate the abnormal toxic effects due to ROS/RNS imbalance, aging, and restoration of the delicate redox hemostasis in brain tissue is the treatment with synthetic and natural neuroprotectants that regulate the redox signaling and signal transduction activities of proteins, lipids, and DNA.
This Research Topic focuses on observing changes in antioxidant expression, identifying ROS/RNS levels, aberration disorders, apoptotic and anti-inflammatory mechanisms after acute or chronic OS, documented in both clinical studies and animal models. Addressing critical issues such as targeted delivery of synthetic and natural neuroprotectants, metal chelators, and combination therapy that neutralizes ROS/RNS and regulates mitochondrial redox modulation, signal transduction, and thus pathophysiology and progression of neurodegenerative disorders, are of great importance.
Original scientific articles, brief reports, hypotheses, and literature reviews describing the role of free radicals in the pathogenesis of oxidant-induced neurodegenerative diseases and monitoring biological markers of OS will be reviewed. We encourage the presentation of research and clinical studies in the field of free radical damage and the identification of biomarkers of oxidative stress, which will contribute to the progress of this complex matter and allow the delineation of future directions of work.
Keywords:
Neurodegeneration, OS, blood-brain barrier, synthetic and natural neuroprotectants, β-amyloid (Aβ), AQP4-dependent glymphatic pathway, targeting toll-like receptor (TLR) pathways, NF-kB, thioredoxin (Trx), thioredoxin reductase (TrxR), signal transduction, ROS/RNS, Ca2+ homeostasis, membrane permeability, lipid peroxidation, protein carbonylation, redox modulation, clinical researches, animal models
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.
Neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, multiple sclerosis, and amyotrophic lateral sclerosis, including acute stroke and age-related chronic disorders are known to result from mutations in membrane potential and cellular homeostasis, part of complex cellular events leading to neurodegeneration and brain disorders.
Intracellular redox-modulatory disturbances caused by oxidative stress (OS) are directly mediated by neuronal pathophysiology, and by the inability of endogenous and exogenous antioxidant defense mechanisms to neutralize accumulating reactive oxygen/nitrogen (ROS/RNS, including nitro-oxidative pathways) species. A potential strategy to regulate the abnormal toxic effects due to ROS/RNS imbalance, aging, and restoration of the delicate redox hemostasis in brain tissue is the treatment with synthetic and natural neuroprotectants that regulate the redox signaling and signal transduction activities of proteins, lipids, and DNA.
This Research Topic focuses on observing changes in antioxidant expression, identifying ROS/RNS levels, aberration disorders, apoptotic and anti-inflammatory mechanisms after acute or chronic OS, documented in both clinical studies and animal models. Addressing critical issues such as targeted delivery of synthetic and natural neuroprotectants, metal chelators, and combination therapy that neutralizes ROS/RNS and regulates mitochondrial redox modulation, signal transduction, and thus pathophysiology and progression of neurodegenerative disorders, are of great importance.
Original scientific articles, brief reports, hypotheses, and literature reviews describing the role of free radicals in the pathogenesis of oxidant-induced neurodegenerative diseases and monitoring biological markers of OS will be reviewed. We encourage the presentation of research and clinical studies in the field of free radical damage and the identification of biomarkers of oxidative stress, which will contribute to the progress of this complex matter and allow the delineation of future directions of work.
Keywords:
Neurodegeneration, OS, blood-brain barrier, synthetic and natural neuroprotectants, β-amyloid (Aβ), AQP4-dependent glymphatic pathway, targeting toll-like receptor (TLR) pathways, NF-kB, thioredoxin (Trx), thioredoxin reductase (TrxR), signal transduction, ROS/RNS, Ca2+ homeostasis, membrane permeability, lipid peroxidation, protein carbonylation, redox modulation, clinical researches, animal models
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.