ArticleExperimental neurology2005
Myelin-associated glycoprotein and complementary axonal ligands, gangliosides, mediate axon stability in the CNS and PNS: neuropathology and behavioral deficits in single- and double-null mice.
Article in Experimental neurology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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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.
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Who cites it
97 citing papers in PubMed, 187 citations in OpenAlex.
- Oligodendrocyte Piezo2 is a regulator of age-dependent myelin integrity and dysregulated in multiple sclerosis.Communications biology · 2026Article
- Metabolic Symbiosis and Vulnerability in the CNS Axon-Myelin Unit.Cellular and molecular neurobiology · 2026Review
- Gangliosides in molecular interactions and cell regulation.The Journal of biological chemistry · 2026Review
- Article
- Prenatal inflammation exacerbates hyperoxia-induced neonatal brain injury.Journal of neuroinflammation · 2025Article
- Age-Related Effects of Inhalational Anesthetics inCurrent issues in molecular biology · 2024Article
- Lipid Rafts: The Maestros of Normal Brain Development.Biomolecules · 2024Review
- Early Intensive Neurorehabilitation in Traumatic Peripheral Nerve Injury-State of the Art.Animals : an open access journal from MDPI · 2024Review
- Functional evaluation of novel variants ofFrontiers in neuroscience · 2024Article
- Gangliosides as Siglec ligands.Glycoconjugate journal · 2023Review
- Treatment with the Glycosphingolipid Modulator THI Rescues Myelin Integrity in the Striatum of R6/2 HD Mice.International journal of molecular sciences · 2023Article
- Myelinodegeneration vs. Neurodegeneration in MS Progressive Forms.International journal of molecular sciences · 2023Article
- The role of gangliosides in the organisation of the node of Ranvier examined in glycosyltransferase transgenic mice.Journal of anatomy · 2022Review
- Aberrant Ganglioside Functions to Underpin Dysregulated Myelination, Insulin Signalling, and Cytokine Expression: Is There a Link and a Room for Therapy?Biomolecules · 2022Review
- Carbohydrate based biomaterials for neural interface applications.Journal of materials chemistry. B · 2022Review
- Start Me Up: How Can Surrounding Gangliosides Affect Sodium-Potassium ATPase Activity and Steer towards Pathological Ion Imbalance in Neurons?Biomedicines · 2022Review
- Application of SygenBioengineering (Basel, Switzerland) · 2022Review
- Ganglioside GM3 Synthase Deficiency in Mouse Models and Human Patients.International journal of molecular sciences · 2022Review
- Plasma Membrane Calcium ATPase-Neuroplastin Complexes Are Selectively Stabilized in GM1-Containing Lipid Rafts.International journal of molecular sciences · 2021Article
- Evaluating Gait and Locomotion in Rodents with the CatWalk.Current protocols · 2021Article
37 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Complementary interacting molecules on myelin and axons are required for long-term axon-myelin stability. Their disruption results in axon degeneration, contributing to the pathogenesis of demyelinating diseases. Myelin-associated glycoprotein (MAG), a minor constituent of central and peripheral nervous system myelin, is a member of the Siglec family of sialic acid-binding lectins and binds to gangliosides GD1a and GT1b, prominent molecules on the axon surface. Mice lacking the ganglioside biosynthetic gene Galgt1 fail to express complex gangliosides, including GD1a and GT1b. In the current studies, CNS and PNS histopathology and behavior of Mag-null, Galgt1-null, and double-null mice were compared on the same mouse strain background. When back-crossed to >99% C57BL/6 strain purity, Mag-null mice demonstrated marked CNS, as well as PNS, axon degeneration, in contrast to prior findings using mice of mixed strain background. On the same background, Mag- and Galgt1-null mice exhibited quantitatively and qualitatively similar CNS and PNS axon degeneration and nearly identical decreases in axon diameter and neurofilament spacing. Double-null mice had qualitatively similar changes. Consistent with these findings, Mag- and Galgt1-null mice had similar motor behavioral deficits, with double-null mice only modestly more impaired. Despite their motor deficits, Mag- and Galgt1-null mice demonstrated hyperactivity, with spontaneous locomotor activity significantly above that of wild type mice. These data demonstrate that MAG and complex gangliosides contribute to axon stability in both the CNS and PNS. Similar neuropathological and behavioral deficits in Galgt1-, Mag-, and double-null mice support the hypothesis that MAG binding to gangliosides contributes to long-term axon-myelin stability.
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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.