ArticleNeurobiology of disease2013
An essential role of MAG in mediating axon-myelin attachment in Charcot-Marie-Tooth 1A disease.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Transcriptional profiling reveals brain region-specific changes in gene expression induced by chronic unpredictable mild stress between stress-susceptible and stress-resilient mice.Psychopharmacology · 2026Article
- Hereditary Polyneuropathies in the Era of Precision Medicine: Genetic Complexity and Emerging Strategies.Genes · 2026Review
- Palmitoylation regulates myelination by modulating the ZDHHC3-Cadm4 axis in the central nervous system.Signal transduction and targeted therapy · 2024Article
- Primary neurolymphomatosis with MAG antibody: a case report.BMC neurology · 2024Article
- Advances of Genome Editing with CRISPR/Cas9 in Neurodegeneration: The Right Path towards Therapy.Biomedicines · 2023Review
- Mechanisms and treatment strategies of demyelinating and dysmyelinating Charcot-Marie-Tooth disease.Neural regeneration research · 2023Review
- Value of Antibody Determinations in Chronic Dysimmune Neuropathies.Brain sciences · 2022Review
- Theophylline Induces Remyelination and Functional Recovery in a Mouse Model of Peripheral Neuropathy.Biomedicines · 2022Article
- Dietary Protein Source Influences Brain Inflammation and Memory in a Male Senescence-Accelerated Mouse Model of Dementia.Molecular neurobiology · 2021Article
- NovelJournal of clinical medicine · 2020Article
- Clinical and Pathological Variation of Charcot-Marie-Tooth 1A in a Large Chinese Cohort.BioMed research international · 2017Article
- Article
- Structural basis of myelin-associated glycoprotein adhesion and signalling.Nature communications · 2016Article
- Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction.eLife · 2016Article
- Myelin-associated inhibitors in axonal growth after CNS injury.Current opinion in neurobiology · 2014Review
- Article
- Axon growth inhibition by RhoA/ROCK in the central nervous system.Frontiers in neuroscience · 2014Review
- MAL overexpression leads to disturbed expression of genes that influence cytoskeletal organization and differentiation of Schwann cells.ASN neuro · 2014Article
- Concepts for regulation of axon integrity by enwrapping glia.Frontiers in cellular neuroscience · 2013Review
- Genetic deletion of Cadm4 results in myelin abnormalities resembling Charcot-Marie-Tooth neuropathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Charcot-Marie-Tooth disease type 1A (CMT1A) is a hereditary demyelinating peripheral neuropathy caused by the duplication of the PMP22 gene. Demyelination precedes the occurrence of clinical symptoms that correlate with axonal degeneration. It was postulated that a disturbed axon-glia interface contributes to altered myelination consequently leading to axonal degeneration. In this study, we examined the expression of MAG and Necl4, two critical adhesion molecules that are present at the axon-glia interface, in sural nerve biopsies of CMT1A patients and in peripheral nerves of mice overexpressing human PMP22, an animal model for CMT1A. We show an increase in the expression of MAG and a strong decrease of Necl4 in biopsies of CMT1A patients as well as in CMT1A mice. Expression analysis revealed that MAG is strongly upregulated during peripheral nerve maturation, whereas Necl4 expression remains very low. Ablating MAG in CMT1A mice results in separation of axons from their myelin sheath. Our data show that MAG is important for axon-glia contact in a model for CMT1A, and suggest that its increased expression in CMT1A disease has a compensatory role in the pathology of the disease. Thus, we demonstrate that MAG together with other adhesion molecules such as Necl4 is important in sustaining axonal integrity.
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