ReviewInternational journal of molecular sciences2023
Synapse Dysfunctions in Multiple Sclerosis.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026Review
- Syntaxin1A in synaptopathies: From molecular mechanisms to therapeutic implications in neurological disorders (Review).Biomedical reports · 2026Review
- MicroRNA-mRNA Regulatory Network Associated with Cognitive Impairment in Multiple Sclerosis.Molecular neurobiology · 2026Article
- Network-based identification of regulatory hubs and therapeutic targets in multiple sclerosis: an integrated transcriptomic and molecular docking approach.Acta neurologica Belgica · 2026Article
- Early Reduction in Mitochondrial Membrane Potential in Synaptic Mitochondria Contribute to Synaptic Pathology in the EAE Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2026Article
- Synaptic Plasticity in Neurodegenerative Diseases: Impact of Exercise as Promising Therapeutic Tool.Cells · 2026Review
- Potential Causal Relationships Between Circulating Micronutrient Levels and Multiple Neuroimmune Diseases: A Genetic Association Analysis.Brain and behavior · 2025Article
- Association of decreased thalamic neurotransmitter level with sensorimotor tract damage in patients with relapsing-remitting multiple sclerosis.Quantitative imaging in medicine and surgery · 2025Article
- Brain Tumors, AI and Psychiatry: Predicting Tumor-Associated Psychiatric Syndromes with Machine Learning and Biomarkers.International journal of molecular sciences · 2025Review
- Cell-specific Nav1.6 knockdown reduced astrocyte-derived Aβ by reverse NaJournal of advanced research · 2025Article
- In Silico Analysis of miRNA-Regulated Pathways in Spinocerebellar Ataxia Type 7.Current issues in molecular biology · 2025Article
- Article
- The effects of Leventhal's self-regulation model-based educational intervention on stress, anxiety, and depression in women with multiple sclerosis: a randomized educational trial.Frontiers in neurology · 2025Article
- Disease-Modifying Symptomatic Treatment (DMST) Potential of Cannabinoids in Patients with Multiple Sclerosis.Current neuropharmacology · 2025Review
- Article
- Interaction between miR-142-3p andInternational journal of molecular sciences · 2024Article
- Pilot Study of the Total and Phosphorylated Tau Proteins in Early-Stage Multiple Sclerosis.Medicina (Kaunas, Lithuania) · 2024Article
- Article
- The Use of Stem Cells as a Potential Treatment Method for Selected Neurodegenerative Diseases: Review.Cellular and molecular neurobiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is a chronic neuroinflammatory disease of the central nervous system (CNS) affecting nearly three million humans worldwide. In MS, cells of an auto-reactive immune system invade the brain and cause neuroinflammation. Neuroinflammation triggers a complex, multi-faceted harmful process not only in the white matter but also in the grey matter of the brain. In the grey matter, neuroinflammation causes synapse dysfunctions. Synapse dysfunctions in MS occur early and independent from white matter demyelination and are likely correlates of cognitive and mental symptoms in MS. Disturbed synapse/glia interactions and elevated neuroinflammatory signals play a central role. Glutamatergic excitotoxic synapse damage emerges as a major mechanism. We review synapse/glia communication under normal conditions and summarize how this communication becomes malfunctional during neuroinflammation in MS. We discuss mechanisms of how disturbed glia/synapse communication can lead to synapse dysfunctions, signaling dysbalance, and neurodegeneration in MS.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.