About this Research Topic
Neurodegenerative diseases, such as Alzheimer's, Parkinson´s, and Amyotrophic Lateral Sclerosis (ALS), share some characteristics with neuroinflammation. Neuroinflammation can be triggered by endogenous components such as neuronal damage, protein misfolding/aggregation, as well as alterations in the clearance mechanisms (damage-associated molecular patterns, DAMPs) or by exogenous components such as pathogens (pathogen-associated molecular patterns, PAMPs). Both DAMPs and PAMPs can be detected by pattern recognition receptors (PRRs) on glial cells whose activation leads to neuroinflammation. During aging, neurodegenerative processes may be associated with failures in clearance processes, protein/peptide aggregation, and the formation of toxic oligomers such as those found in senile plaques.
Furthermore, protein dysregulation, mainly involving kinases and transcription factors, is also found in neuroinflammation. Protein dysregulation can occur at the transcriptional level; at translational level; and at the post-translational level. Alterations in these mechanisms can cause neurodegeneration and even lead to a neuronal-cell invasive phenotype and oncologycal processes.
This Research Topic focuses on novel investigations of metabolic alterations and molecular pathways in neuroinflammation and neurodegeneration associated with aging. This topic also considers research on malignant tumors that develop in the central nervous system in aging.
We welcome the submissions of original research and reviews that cover the following areas, but are not limited to:
• Proteostasis and clearance of pathological oligomers
• Neuro-oncology associated with aging
• Signal transduction pathways in the brain aging
• Molecular mechanisms in the brain during aging
• Clearance of pathological oligomers
• Microglial pathologies and their role in neurodegeneration
• Anti-inflammatory drugs as therapeutic molecules against neurodegeneration
• Homeostasis of microglia in the health of the old brain
• Cytokines and neuronal damage
Furthermore, protein dysregulation, mainly involving kinases and transcription factors, is also found in neuroinflammation. Protein dysregulation can occur at the transcriptional level; at translational level; and at the post-translational level. Alterations in these mechanisms can cause neurodegeneration and even lead to a neuronal-cell invasive phenotype and oncologycal processes.
This Research Topic focuses on novel investigations of metabolic alterations and molecular pathways in neuroinflammation and neurodegeneration associated with aging. This topic also considers research on malignant tumors that develop in the central nervous system in aging.
We welcome the submissions of original research and reviews that cover the following areas, but are not limited to:
• Proteostasis and clearance of pathological oligomers
• Neuro-oncology associated with aging
• Signal transduction pathways in the brain aging
• Molecular mechanisms in the brain during aging
• Clearance of pathological oligomers
• Microglial pathologies and their role in neurodegeneration
• Anti-inflammatory drugs as therapeutic molecules against neurodegeneration
• Homeostasis of microglia in the health of the old brain
• Cytokines and neuronal damage
Keywords: Protein/peptide aggregation, neuroinflammation, M1 and M2 microglia, cytokines, neuro- oncology, molecular mechanisms, signaling pathways, brain aging
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.
