Neuroinflammation is a prominent feature observed in numerous acute lesions and neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and age-related degeneration affecting sensory functions such as vision, hearing, and olfaction. However, the precise role of neuroinflammation in the process of remyelination remains elusive. Both innate and adaptive immune mechanisms are believed to be crucial for facilitating successful remyelination. Specifically, microglial cells and macrophages within the central nervous system (CNS) have been identified as key modulators involved in the remyelination process following CNS damage. In the peripheral nervous system, mediation is primarily carried out by macrophages, neutrophils, monocytes, among others. Acute neuroinflammatory responses typically manifest in response to neural injury, infections, toxin exposure, or under autoimmune conditions. Transient neuroinflammatory signaling plays a protective role during developmental and post-injury tissue repair, while chronic neuroinflammation is associated with the progression of demyelinating diseases such as Alzheimer's, Parkinson's, and age-related neurodegeneration. Pathological neuroinflammation related to neurodegeneration is predominantly mediated by microglial cells and macrophages. However, the precise roles of microglial cells and macrophages in mediating neuroinflammation during acute and chronic degenerative processes remain poorly understood. This proposed research topic aims to investigate the specific roles of microglial cells and macrophages in mediating acute and chronic neuroinflammation in demyelination, thereby providing novel theoretical insights for the development of treatment strategies targeting neuroinflammation.
The principal aim of this research initiative is to elucidate novel insights into the intricate mechanisms underlying neuroinflammation, specifically mediated by innate and adaptive immune responses, in the pathogenesis of neurodegenerative diseases. Furthermore, the study endeavors to explore potential therapeutic targets for demyelinating disorders within this context. The thematic areas encompass a broad spectrum, including but not limited to:
1. Neuroinflammation orchestrated by innate and adaptive immunity, encompassing an array of cellular constituents such as mast cells, macrophages, neutrophils, and dendritic cells.
2. Intracellular signaling pathways modulating the crosstalk between oligodendrocytes and microglia.
3. Molecular and cytokine signaling cascades intricately regulating the functionality of myelinated nerve fibers.
4. Elucidation of the underlying mechanisms governing the role of neural stem cells in the pathophysiology of neurodegenerative processes.
5. Examination of the influence exerted by gut microbiota and their metabolites on the etiology and progression of neurodegenerative diseases.
6. Identification and validation of circulating biomarkers within the hematological system predictive of the prognostic outcomes of neurodegenerative lesions.
7. Investigation into the systemic repercussions of functional alterations in peripheral organs on the trajectory of neurodegenerative disorders.
Studies addressing these complex mechanisms through a comprehensive array of in vitro and in vivo methodologies are strongly encouraged. The submission of scholarly contributions, including original research articles, comprehensive reviews, systematic reviews, meta-analyses, and in-depth mini-reviews, offering profound insights into the evolving landscape of neuroinflammation and demyelinating disorders in the context of neurodegenerative diseases, is eagerly anticipated. Moreover, there is a keen interest in the integration of histopathological techniques to present compelling clinical case reports elucidating neuroinflammatory responses intertwined with the intricate interplay of the gut-brain axis, kidney-brain axis, and other pertinent pathways.
Keywords:
Neuroinflammation, Remyelination, Aging, Neurodegeneration, Neurological Diseases, Alzheimer's Diseases
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.
Neuroinflammation is a prominent feature observed in numerous acute lesions and neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and age-related degeneration affecting sensory functions such as vision, hearing, and olfaction. However, the precise role of neuroinflammation in the process of remyelination remains elusive. Both innate and adaptive immune mechanisms are believed to be crucial for facilitating successful remyelination. Specifically, microglial cells and macrophages within the central nervous system (CNS) have been identified as key modulators involved in the remyelination process following CNS damage. In the peripheral nervous system, mediation is primarily carried out by macrophages, neutrophils, monocytes, among others. Acute neuroinflammatory responses typically manifest in response to neural injury, infections, toxin exposure, or under autoimmune conditions. Transient neuroinflammatory signaling plays a protective role during developmental and post-injury tissue repair, while chronic neuroinflammation is associated with the progression of demyelinating diseases such as Alzheimer's, Parkinson's, and age-related neurodegeneration. Pathological neuroinflammation related to neurodegeneration is predominantly mediated by microglial cells and macrophages. However, the precise roles of microglial cells and macrophages in mediating neuroinflammation during acute and chronic degenerative processes remain poorly understood. This proposed research topic aims to investigate the specific roles of microglial cells and macrophages in mediating acute and chronic neuroinflammation in demyelination, thereby providing novel theoretical insights for the development of treatment strategies targeting neuroinflammation.
The principal aim of this research initiative is to elucidate novel insights into the intricate mechanisms underlying neuroinflammation, specifically mediated by innate and adaptive immune responses, in the pathogenesis of neurodegenerative diseases. Furthermore, the study endeavors to explore potential therapeutic targets for demyelinating disorders within this context. The thematic areas encompass a broad spectrum, including but not limited to:
1. Neuroinflammation orchestrated by innate and adaptive immunity, encompassing an array of cellular constituents such as mast cells, macrophages, neutrophils, and dendritic cells.
2. Intracellular signaling pathways modulating the crosstalk between oligodendrocytes and microglia.
3. Molecular and cytokine signaling cascades intricately regulating the functionality of myelinated nerve fibers.
4. Elucidation of the underlying mechanisms governing the role of neural stem cells in the pathophysiology of neurodegenerative processes.
5. Examination of the influence exerted by gut microbiota and their metabolites on the etiology and progression of neurodegenerative diseases.
6. Identification and validation of circulating biomarkers within the hematological system predictive of the prognostic outcomes of neurodegenerative lesions.
7. Investigation into the systemic repercussions of functional alterations in peripheral organs on the trajectory of neurodegenerative disorders.
Studies addressing these complex mechanisms through a comprehensive array of in vitro and in vivo methodologies are strongly encouraged. The submission of scholarly contributions, including original research articles, comprehensive reviews, systematic reviews, meta-analyses, and in-depth mini-reviews, offering profound insights into the evolving landscape of neuroinflammation and demyelinating disorders in the context of neurodegenerative diseases, is eagerly anticipated. Moreover, there is a keen interest in the integration of histopathological techniques to present compelling clinical case reports elucidating neuroinflammatory responses intertwined with the intricate interplay of the gut-brain axis, kidney-brain axis, and other pertinent pathways.
Keywords:
Neuroinflammation, Remyelination, Aging, Neurodegeneration, Neurological Diseases, Alzheimer's Diseases
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.