Observational studyNeuropathology and applied neurobiology2022
MiR-142-3p regulates synaptopathy-driven disease progression in multiple sclerosis.
Observational study in Neuropathology and applied neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Targeting the Gut Dysbiosis to Treat Inflammation-driven Synaptopathy in Multiple Sclerosis
Transcranial Static Field Stimulation (tSMS) and Transcranial Direct Current Stimulation (tDCS) for the Treatment of Neurological Symptoms
Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Cerebrospinal fluid amino acid alterations are associated with oxidative stress and neuronal injury markers in multiple sclerosis.Metabolic brain disease · 2026Article
- Longitudinal and Stability-Aware Analysis Reveals Treatment-Specific MicroRNA Response Signatures Following Immune-Reconstitution and B-Cell-Targeted Therapies in Multiple Sclerosis.International journal of molecular sciences · 2026Article
- MicroRNAs as Biomarkers for the Diagnosis and Prognosis of Different Diseases and Cancer.Experientia supplementum (2012) · 2026Review
- From Molecules to Models: miRNAs and Advanced Human Platforms of Neurodegeneration and Repair in Multiple Sclerosis.International journal of molecular sciences · 2025Review
- Targeted miRNA Delivery in Epilepsy: Mechanisms, Advances, and Therapeutic Potential.Molecular biology reports · 2025Review
- ADAR1-regulated miR-142-3p/RIG-I axis suppresses antitumor immunity in nasopharyngeal carcinoma.Non-coding RNA research · 2025Article
- Short-term exposure to particulate matter triggers a selective alteration of plasma extracellular vesicle-packaged miRNAs in a mouse model of multiple sclerosis.Frontiers in immunology · 2025Article
- Circulating miRNAs in the Plasma of Post-COVID-19 Patients with Typical Recovery and Those with Long-COVID Symptoms: Regulation of Immune Response-Associated Pathways.Non-coding RNA · 2024Article
- [Expression of miR-142 and its relationship with Th17/Treg imbalance in children with autoimmune thyroid disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Interleukin-9 protects from microglia- and TNF-mediated synaptotoxicity in experimental multiple sclerosis.Journal of neuroinflammation · 2024Article
- Interaction between miR-142-3p andInternational journal of molecular sciences · 2024Article
- Regulatory role of the miR-142-3p/Translational lung cancer research · 2024Article
- Multiple Sclerosis: Roles of miRNA, lcnRNA, and circRNA and Their Implications in Cellular Pathways.International journal of molecular sciences · 2024Review
- MiRNA-based therapeutic potential in multiple sclerosis.Frontiers in immunology · 2024Review
- Interleukin-10 contrasts inflammatory synaptopathy and central neurodegenerative damage in multiple sclerosis.Frontiers in molecular neuroscience · 2024Article
- miRNAs: Targets to Investigate Herpesvirus Infection Associated with Neurological Disorders.International journal of molecular sciences · 2023Review
- Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration.Journal of biomedical science · 2023Review
- Experimental encephalomyelitis at age 90, still relevant and elucidating how viruses trigger disease.The Journal of experimental medicine · 2023Article
- Shared miRNA landscapes of COVID-19 and neurodegeneration confirm neuroinflammation as an important overlapping feature.Frontiers in molecular neuroscience · 2023Article
- MiR-142-3p is a Critical Modulator of TNF-mediated Neuronal Toxicity in Multiple Sclerosis.Current neuropharmacology · 2023Article
Corrections and comments
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Authors and funding
31 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimWe recently proposed miR-142-3p as a molecular player in inflammatory synaptopathy, a new pathogenic hallmark of multiple sclerosis (MS) and of its mouse model experimental autoimmune encephalomyelitis (EAE), that leads to neuronal loss independently of demyelination. MiR-142-3p seems to be unique among potential biomarker candidates in MS, since it is an inflammatory miRNA playing a dual role in the immune and central nervous systems. Here, we aimed to verify the impact of miR-142-3p circulating in the cerebrospinal fluid (CSF) of MS patients on clinical parameters, neuronal excitability and its potential interaction with disease modifying therapies (DMTs). METHODS AND
resultsIn a cohort of 151 MS patients, we found positive correlations between CSF miR-142-3p levels and clinical progression, IL-1β signalling as well as synaptic excitability measured by transcranial magnetic stimulation. Furthermore, therapy response of patients with 'low miR-142-3p' to dimethyl fumarate (DMF), an established disease-modifying treatment (DMT), was superior to that of patients with 'high miR-142-3p' levels. Accordingly, the EAE clinical course of heterozygous miR-142 mice was ameliorated by peripheral DMF treatment with a greater impact relative to their wild type littermates. In addition, a central protective effect of this drug was observed following intracerebroventricular and ex vivo acute treatments of EAE wild type mice, showing a rescue of miR-142-3p-dependent glutamatergic alterations. By means of electrophysiology, molecular and biochemical analysis, we suggest miR-142-3p as a molecular target of DMF.
conclusionMiR-142-3p is a novel and potential negative prognostic CSF marker of MS and a promising tool for identifying personalised therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.