ReviewNature reviews. Neurology2015
Synaptopathy connects inflammation and neurodegeneration in multiple sclerosis.
Review in Nature reviews. Neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 5 registered trials, which are not on this map. Cited by 149 papers, 1 of them a synthesis that pooled it.
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.
Clinical Relevance of miR-142-3p as Potential Biomarker of Synaptopathy in Multiple Sclerosis
Interventional Not Pharmacological Study to Investigate the Role of ADA in Multiple Sclerosis PatientsTreated With an Immune-Reconstitution Therapy (2-CdA)
Study on the Interaction Between Immune, Autonomic and Central Nervous Systems as a Target of Exercise Therapy in Multiple Sclerosis
Effects of Ozanimod on Immune-mediated Mechanisms of Neurodegeneration in Multiple Sclerosis - a Preclinical Study
Targeting the Gut Dysbiosis to Treat Inflammation-driven Synaptopathy in Multiple Sclerosis
Who cites it
149 citing papers in PubMed, 1 synthesis or guideline pooled it, 299 citations in OpenAlex.
- Genes associated with grey matter volume reduction in multiple sclerosis.Journal of neurology · 2022Pooled it
- CSF Cytokine Network Organization Predicts Progression Independent of Relapse and MRI Activity in Multiple Sclerosis.Annals of clinical and translational neurology · 2026Article
- Sleep Macrostructure, Cyclic Alternating Pattern and CSF Cytokines in De Novo Relapsing-Remitting Multiple Sclerosis: A Controlled Polysomnographic Study.Journal of sleep research · 2026Article
- Review
- 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
- SV2A PET reveals synaptic density loss in experimental autoimmune encephalomyelitis and in a pilot multiple sclerosis study.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Serum metabolomic-lipidomic signatures track long-term neurological performance in multiple sclerosis.Molecular neurodegeneration advances · 2026Article
- TMS-EEG signatures of motor network dysfunction in multiple sclerosis.Brain communications · 2026Article
- Gut-derived memory T cells: key mediators of neuroinflammation via the gut-brain axis.Frontiers in medicine · 2026Review
- β-Endorphin Mediates Electroacupuncture-Induced Remyelination via Neural Stem Cell Lineage Modulation in Experimental Autoimmune Encephalomyelitis.CNS neuroscience & therapeutics · 2025Article
- Neuron-Derived Extracellular Vesicles: Emerging Regulators in Central Nervous System Disease Progression.Molecular neurobiology · 2025Review
- Changes in circulating pro-inflammatory lymphocytes and cortical excitability with extended-interval natalizumab dosing in multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- Letter to the Editor: "VEP Latency Delay Reflects Demyelination Beyond the Optic Nerve in the Cuprizone Model".Investigative ophthalmology & visual science · 2025Article
- Neuronal Plasticity-Dependent Paradigm and Young Plasma Treatment Prevent Synaptic and Motor Deficit in a Rett Syndrome Mouse Model.Biomolecules · 2025Article
- CRISPR-based epigenetic editing of Gad1 improves synaptic inhibition and cognitive behavior in a Tauopathy mouse model.Neurobiology of disease · 2025Article
- Astroglial modulation of synaptic function in the non-demyelinated cerebellar cortex is dependent on MyD88 signaling in a model of toxic demyelination.Journal of neuroinflammation · 2025Article
- Article
- Unraveling the inflammation-degeneration tangle in early MS: preliminary insights from ferritin, neurogranin, TREM2, and retinal ganglion cell layer.Journal of neurology · 2025Article
- Ginsenoside Rk1 alleviates lipopolysaccharide (LPS)-induced cognitive impairment by modulating synaptic plasticity.Frontiers in pharmacology · 2025Article
- Disease-Modifying Symptomatic Treatment (DMST): The Potential Role of Vortioxetine in the Treatment of Depression in Patients with Multiple Sclerosis.Current neuropharmacology · 2025Review
89 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) has long been regarded as a chronic inflammatory disease of the white matter that leads to demyelination and eventually to neurodegeneration. In the past decade, several aspects of MS pathogenesis have been challenged, and degenerative changes of the grey matter, which are independent of demyelination, have become a topic of interest. CNS inflammation in MS and experimental autoimmune encephalomyelitis (EAE; a disease model used to study MS in rodents) causes a marked imbalance between GABAergic and glutamatergic transmission, and a loss of synapses, all of which leads to a diffuse 'synaptopathy'. Altered synaptic transmission can occur early in MS and EAE, independently of demyelination and axonal loss, and subsequently causes excitotoxic damage. Inflammation-driven synaptic abnormalities are emerging as a prominent pathogenic mechanism in MS-importantly, they are potentially reversible and, therefore, represent attractive therapeutic targets. In this Review, we focus on the connection between inflammation and synaptopathy in MS and EAE, which sheds light not only on the pathophysiology of MS but also on that of primary neurodegenerative disorders in which inflammatory processes contribute to disease progression.
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Identifiers
What OpenQuestion 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 OpenQuestion graph.