ArticleJournal of neuroinflammation2023
N-acetylglucosamine inhibits inflammation and neurodegeneration markers in multiple sclerosis: a mechanistic trial.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- The Crossroads of Neuroinflammation and Biomarkers in Multiple Sclerosis: A Systematic Review.Cells · 2026Pooled it
- CAR-T Cell Therapy and Gut Microbiota Modulation in Multiple Sclerosis: Emerging Therapeutic Strategies and Current Limitations.Current issues in molecular biology · 2026Review
- Aegle marmelos neuroprotective potential in demyelination rat model through modulation of BDNF, GDNF, HSP-90 and HSP-60.Inflammopharmacology · 2026Article
- Roles of cerebrospinal fluid metabolites in neuromyelitis optica spectrum disorder: Insights from Mendelian randomization.Medicine · 2026Article
- Glucosamine/chitosan blend surface-engineered rutin-loaded polymer/lipid hybrid nanoparticles for neuroprotection in induced schizophrenia model.Scientific reports · 2026Article
- Advancing MSC-EV Therapies: Harnessing Preconditioning and Mito-EVs to Tackle Neuroinflammation and Neurodegeneration.Pharmaceutics · 2026Review
- Genetic Rescue of Pathogenic O-GlcNAc Dyshomeostasis Associated with Microcephaly and Motor Deficits.eNeuro · 2026Article
- N-Acetylglucosamine Selectively Attenuates Neuroinflammation in a Mouse Model of Mitochondrial Dysfunction.Acta physiologica (Oxford, England) · 2026Article
- N-glycomics profiling reveals alteration of fucosylation in early acute ischemic stroke from mouse brain tissue to human serum.Clinical proteomics · 2026Article
- Article
- PlasmaNeurology(R) neuroimmunology & neuroinflammation · 2025Article
- Improvement of Spontaneous Locomotor Activity in a Murine Model of Duchenne Muscular Dystrophy by N-Acetylglucosamine Alone and in Combination With Prednisolone.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Glycosylation in neuroinflammation: mechanisms, implications, and therapeutic strategies for neurodegenerative diseases.Translational neurodegeneration · 2025Review
- The Oncometabolite 2-Hydroxyglutarate Is Upregulated in Post-Prostatectomy PSA Recurrence of Prostate Cancer: A Metabolomic Analysis.Molecules (Basel, Switzerland) · 2025Article
- Effect of Platelet-Derived Microparticles on the Expression of Adhesion Molecules in Endothelial Cells.International journal of molecular sciences · 2025Article
- IgG N-glycosylation contributes to different severities of insulin resistance: implications for 3P medical approaches.The EPMA journal · 2025Article
- Dynamic glycosylation remodeling in neurological disorders.Frontiers in molecular neuroscience · 2025Review
- Serum glycobiomarkers for chronic inflammatory demyelinating polyneuropathy.European journal of neurology · 2025Article
- N-Glycan Branching Regulates BTLA Opposite to PD-1 to Limit T Cell Hyperactivity Induced by Branching Deficiency.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The Immunometabolic Gene N-Acetylglucosamine Kinase Is Uniquely Involved in the Heritability of Multiple Sclerosis Severity.International journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundIn the demyelinating disease multiple sclerosis (MS), chronic-active brain inflammation, remyelination failure and neurodegeneration remain major issues despite immunotherapy. While B cell depletion and blockade/sequestration of T and B cells potently reduces episodic relapses, they act peripherally to allow persistence of chronic-active brain inflammation and progressive neurological dysfunction. N-acetyglucosamine (GlcNAc) is a triple modulator of inflammation, myelination and neurodegeneration. GlcNAc promotes biosynthesis of Asn (N)-linked-glycans, which interact with galectins to co-regulate the clustering/signaling/endocytosis of multiple glycoproteins simultaneously. In mice, GlcNAc crosses the blood brain barrier to raise N-glycan branching, suppress inflammatory demyelination by T and B cells and trigger stem/progenitor cell mediated myelin repair. MS clinical severity, demyelination lesion size and neurodegeneration inversely associate with a marker of endogenous GlcNAc, while in healthy humans, age-associated increases in endogenous GlcNAc promote T cell senescence. OBJECTIVES AND
methodsAn open label dose-escalation mechanistic trial of oral GlcNAc at 6 g (n = 18) and 12 g (n = 16) for 4 weeks was performed in MS patients on glatiramer acetate and not in relapse from March 2016 to December 2019 to assess changes in serum GlcNAc, lymphocyte N-glycosylation and inflammatory markers. Post-hoc analysis examined changes in serum neurofilament light chain (sNfL) as well as neurological disability via the Expanded Disability Status Scale (EDSS).
resultsPrior to GlcNAc therapy, high serum levels of the inflammatory cytokines IFNγ, IL-17 and IL-6 associated with reduced baseline levels of a marker of endogenous serum GlcNAc. Oral GlcNAc therapy was safe, raised serum levels and modulated N-glycan branching in lymphocytes. Glatiramer acetate reduces T
conclusionsOral GlcNAc inhibits inflammation and neurodegeneration markers in MS patients despite concurrent immunomodulation by glatiramer acetate. Blinded studies are required to investigate GlcNAc's potential to control residual brain inflammation, myelin repair and neurodegeneration in MS.
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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.