Oxidative stress, free radicals, antioxidants - when it comes to our health, this topic is taking up more and more attention. But what is oxidative stress, how does it arise and what effects does it have on the most sensitive area of our body: the neuronal tissue or the retina. Many neurological diseases affecting the brain or the retina are associated with elevated levels of reactive oxygen species (ROS).
High levels of ROS can cause damage to proteins, nucleic acids, lipids, membranes, and organelles such as mitochondria, and can be caused not only by external stimuli but also by aging. Most theories on the aging scenario assume that cumulative oxidative stress leads to mitochondrial changes, mitochondrial dysfunction, and oxidative damage. Therefore, it is not surprising that excess ROS is among others associated with the development of a variety of age-related neuronal diseases, including Alzheimer's and Parkinson's disease, as well as retinal diseases diabetic retinopathy, glaucoma, and age-related macular (AMD) degeneration.
The aim of this Research Topic is to answer open questions, to combine already gained knowledge, to close the gaps between ophthalmology and neurology when it comes to oxidative stress in order to understand the underlying pathways and derive innovative therapies. It searches for the updates and new findings in both fields that answer the central question: are the same cell types affected by oxidative stress in the same way in the brain and retina? Experimental studies or patient studies that provide new insights are welcome, as well as studies that investigate antioxidant therapies.
We encourage submissions that aim to bridge the gap between ophthalmology and neurology, i.e. papers examining cell types involved in oxidative stress in the retina and the brain. Open questions like the following should be addressed:
· What is the difference at the molecular and pathological level between diseases associated with oxidative stress in the retina and in the brain?
· Does it always occur with age?
· If oxidative stress is truly fundamental to pathogenesis, why has the use of antioxidants been largely unsuccessful in such diseases?
· When are ROS useful and when are they harmful?
· It is known that ROS play an important role in immune defense and signal transduction. What induces the pathogenesis, is it the amount or the type of ROS?
· Do the molecular pathomechanisms differ between neurodegenerative diseases and are they also present in congenital diseases?
· What role do different cell types such as micro- or macroglia, amacrine or bipolar, or RPE cells play in the retina?
· Which cell types are the key players in the brain?
· Novel therapeutic approaches for oxidative stress?
· There are numerous inhibitors, diets, neuroprotective compounds, anti-inflammatories but why are most of them insufficient?
· What is the impact of ROS on disease onset, pathogenesis, and therapy (mitochondrial, plasma membrane, or cytosol ROS)?
Oxidative stress, free radicals, antioxidants - when it comes to our health, this topic is taking up more and more attention. But what is oxidative stress, how does it arise and what effects does it have on the most sensitive area of our body: the neuronal tissue or the retina. Many neurological diseases affecting the brain or the retina are associated with elevated levels of reactive oxygen species (ROS).
High levels of ROS can cause damage to proteins, nucleic acids, lipids, membranes, and organelles such as mitochondria, and can be caused not only by external stimuli but also by aging. Most theories on the aging scenario assume that cumulative oxidative stress leads to mitochondrial changes, mitochondrial dysfunction, and oxidative damage. Therefore, it is not surprising that excess ROS is among others associated with the development of a variety of age-related neuronal diseases, including Alzheimer's and Parkinson's disease, as well as retinal diseases diabetic retinopathy, glaucoma, and age-related macular (AMD) degeneration.
The aim of this Research Topic is to answer open questions, to combine already gained knowledge, to close the gaps between ophthalmology and neurology when it comes to oxidative stress in order to understand the underlying pathways and derive innovative therapies. It searches for the updates and new findings in both fields that answer the central question: are the same cell types affected by oxidative stress in the same way in the brain and retina? Experimental studies or patient studies that provide new insights are welcome, as well as studies that investigate antioxidant therapies.
We encourage submissions that aim to bridge the gap between ophthalmology and neurology, i.e. papers examining cell types involved in oxidative stress in the retina and the brain. Open questions like the following should be addressed:
· What is the difference at the molecular and pathological level between diseases associated with oxidative stress in the retina and in the brain?
· Does it always occur with age?
· If oxidative stress is truly fundamental to pathogenesis, why has the use of antioxidants been largely unsuccessful in such diseases?
· When are ROS useful and when are they harmful?
· It is known that ROS play an important role in immune defense and signal transduction. What induces the pathogenesis, is it the amount or the type of ROS?
· Do the molecular pathomechanisms differ between neurodegenerative diseases and are they also present in congenital diseases?
· What role do different cell types such as micro- or macroglia, amacrine or bipolar, or RPE cells play in the retina?
· Which cell types are the key players in the brain?
· Novel therapeutic approaches for oxidative stress?
· There are numerous inhibitors, diets, neuroprotective compounds, anti-inflammatories but why are most of them insufficient?
· What is the impact of ROS on disease onset, pathogenesis, and therapy (mitochondrial, plasma membrane, or cytosol ROS)?
