ReviewCellular and molecular neurobiology2025
MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis.
Review in Cellular and molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Shedding Light on Interaction Between Neurological Symptoms and Psychiatric Episodes in Multiple Sclerosis: Novel Hypothesis and Therapeutic Avenues.Molecular neurobiology · 2026Review
- Neuroinflammation and Secretase Regulation in Alzheimer's Disease: From Molecular Cross-Talk to Multi-Target Therapeutics.International journal of molecular sciences · 2026Review
- Multifaceted roles of miR‑124 in cancer: Molecular mechanisms and clinical prospects (Review).International journal of oncology · 2026Review
- Microglial Plasticity in Vascular Dementia: Mechanisms and Therapeutic Reprogramming.International journal of molecular sciences · 2026Review
- Serum miRNA-155 and TREM2 as Non-Invasive Biomarkers for Monitoring Neuroinflammation and Disease Activity in Multiple Sclerosis.Molecular neurobiology · 2026Review
- Mapping the Ischemic Continuum: Dynamic Multi-Omic Biomarker and AI for Personalized Stroke Care.International journal of molecular sciences · 2026Review
- Reprogramming brain-resident macrophages: from disease drivers to therapeutic allies in neurological disorders.Frontiers in cellular neuroscience · 2026Review
- Neuroinflammation and treatment resistance in major depressive disorder.Frontiers in pharmacology · 2026Review
- Molecular Interplay Between COVID-19 and Stroke: Experimental Insights Into MicroRNA-Regulated Neuroinflammation.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026Article
- Extracellular RNAs as Messengers and Early Biomarkers in Neurodegeneration.International journal of molecular sciences · 2025Review
- Neurovascular Dysfunction and Glymphatic Impairment: An Unexplored Therapeutic Frontier in Neurodegeneration.International journal of molecular sciences · 2025Review
- Extracellular vesicle-based therapies for neurodegenerative diseases.NeuroImmune pharmacology and therapeutics · 2025Review
- Non-coding RNAs in Parkinson's Disease: Pathogenesis, Exosomes, and Therapeutic Horizons.Cellular and molecular neurobiology · 2025Review
- Insights into the Versatile Role of Extracellular Vesicles in the Treatment of CNS Disorders.Molecular neurobiology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease associated with demyelination and microglial activation. Significant progress has recently been made in the development of strategies to treat MS with a focus on microglial cells. In response to injury, microglia, a population of mononuclear phagocytic cells, change from quiescent to activated. M1 microglia produce pro-inflammatory cytokines that cause additional injury, thus they are considered neurotoxic microglia. M2 microglia release anti-inflammatory factors that lead to the suppression of inflammatory responses; therefore, they have a neurotrophic phenotype. The balance between M1 and M2 phenotypes is important for nerve recovery. In neurodegenerative diseases, activated microglia are excessively shifted toward M1 or neurotoxic phenotype due to microRNA (miRNA) dysregulation. The miRNA as a class of non-coding RNAs, control the neuroinflammatory process by activation of microglia. The miR-124 is partly responsible for suppressing the neuroprotective and inflammatory processes by preventing microglia activation. Meanwhile, the microRNA 155, which is induced by pro-inflammatory agents in microglia, promotes the inflammatory process. Several studies have shown that in MS pathogenesis, miR-124 as an anti-inflammatory marker is significantly downregulated, while miR-155 shows an increase. In this study, we will investigate the role of miR-124 and miR-155 in the activation and alteration of microglial phenotype. Finding the relationship between microRNAs and glial cells and inflammation in MS may be used as a therapeutic method to reduce the symptoms in MS patients.
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