About this Research Topic
Neuroinflammation is a primary hallmark in several myelin-related disorders, namely Multiple Sclerosis, and has long been associated with demyelination and remyelination. Several studies suggest that modulation of inflammatory events may be the most effective means to enhance remyelination.
Release of inflammatory molecules have been described in several myelin-related disorders, which can be detected either in serum or in the CSF of patients, however none have yet been proven to carry sufficient predictive reliability for routine clinical use for disease diagnosis or prognosis.
Although the majority of neuroinflammation research has focussed on the invasion of the Central Nervous System by immune cells derived from the periphery, recent data highlight the crucial role of glial cells, namely astrocytes and microglia, in the set of the inflammatory milieu upon damage.
Most attractive is the fact that these cells shift their phenotype and function along disease course, being implicated in myelin repair mechanisms. Dysregulation of astro- and microglial activation / function may thus regulate the efficiency of remyelination.
To cover these emerging themes, articles focusing on the following issues are welcome in this Frontiers Research Topic:
I: New inflammatory molecules as potential biomarkers of myelin damage
We aim to provide a comprehensive overview of the most recent findings in molecular neuroinflammation in the context of myelin damage. To ascertain whether the presence of inflammatory molecules, either in the serum or CSF of patients with myelin disorders, may improve disease diagnosis, prognosis or treatment efficacy.
II: Targeting inflammatory molecules to improve myelin repair
Submitted articles will describe new crucial molecular players in myelin damage or repair, and explain the mechanisms behind their targeting for efficient remyelination.
III: Role of glial cells in myelin damage and repair
Manuscripts will focus on the role of glial cells and their activation during myelin damage and repair. Further description on diversity and dynamics of glial cell phenotypes and their functional properties during myelin damage and repair may open new avenues for new therapeutic interventions.
Release of inflammatory molecules have been described in several myelin-related disorders, which can be detected either in serum or in the CSF of patients, however none have yet been proven to carry sufficient predictive reliability for routine clinical use for disease diagnosis or prognosis.
Although the majority of neuroinflammation research has focussed on the invasion of the Central Nervous System by immune cells derived from the periphery, recent data highlight the crucial role of glial cells, namely astrocytes and microglia, in the set of the inflammatory milieu upon damage.
Most attractive is the fact that these cells shift their phenotype and function along disease course, being implicated in myelin repair mechanisms. Dysregulation of astro- and microglial activation / function may thus regulate the efficiency of remyelination.
To cover these emerging themes, articles focusing on the following issues are welcome in this Frontiers Research Topic:
I: New inflammatory molecules as potential biomarkers of myelin damage
We aim to provide a comprehensive overview of the most recent findings in molecular neuroinflammation in the context of myelin damage. To ascertain whether the presence of inflammatory molecules, either in the serum or CSF of patients with myelin disorders, may improve disease diagnosis, prognosis or treatment efficacy.
II: Targeting inflammatory molecules to improve myelin repair
Submitted articles will describe new crucial molecular players in myelin damage or repair, and explain the mechanisms behind their targeting for efficient remyelination.
III: Role of glial cells in myelin damage and repair
Manuscripts will focus on the role of glial cells and their activation during myelin damage and repair. Further description on diversity and dynamics of glial cell phenotypes and their functional properties during myelin damage and repair may open new avenues for new therapeutic interventions.
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.
