ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016
Neurodegeneration Triggers Peripheral Immune Cell Recruitment into the Forebrain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Effects of Sphingosine 1-phosphate Modulators on Central Remyelination: A Systematic Review of Animal Models.Cellular and molecular neurobiology · 2026Pooled it
- CLIC1 Protein Accumulates in Circulating Monocyte Membrane during Neurodegeneration.International journal of molecular sciences · 2020Trial
- CD44 as a Conserved Biomarker and Functional Modulator of Neuroinflammation in Multiple Sclerosis and Beyond.Molecular neurobiology · 2026Article
- Astrocytic Accumulation at the Choroid Plexus Attachment Region.Cellular and molecular neurobiology · 2026Article
- Insights and challenges on animal models for progressive multiple sclerosis.Journal of neuroinflammation · 2026Review
- Proteomic Characterization of Spinal Cord Myelin in the Mouse.ASN neuro · 2026Article
- Niraparib Demonstrates Therapeutic Potential in Multiple Sclerosis through Inhibition of IL-17A Receptor Interaction and Promotion of Remyelination.ACS chemical neuroscience · 2025Article
- Article
- N-butyl-β-carboline-3-carboxylate (β-CCB) systemic administration promotes remyelination in the cuprizone demyelinating model in mice.Scientific reports · 2024Article
- How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024Review
- The Heterogeneous Multiple Sclerosis Lesion: How Can We Assess and Modify a Degenerating Lesion?International journal of molecular sciences · 2023Review
- Imaging immunomodulatory treatment responses in a multiple sclerosis mouse model using hyperpolarizedCommunications medicine · 2023Article
- Neurodegeneration and its potential markers in the diagnosing of secondary progressive multiple sclerosis. A review.Frontiers in molecular neuroscience · 2023Review
- Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022Review
- Siponimod ameliorates metabolic oligodendrocyte injury via the sphingosine-1 phosphate receptor 5.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Motor Behavioral Deficits in the Cuprizone Model: Validity of the Rotarod Test Paradigm.International journal of molecular sciences · 2022Review
- Proteomics in Multiple Sclerosis: The Perspective of the Clinician.International journal of molecular sciences · 2022Review
- Sexual Dimorphism in Extracellular Matrix Composition and Viscoelasticity of the Healthy and Inflamed Mouse Brain.Biology · 2022Article
- Animal models to investigate the effects of inflammation on remyelination in multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
- Mechanistic Insights Into Gut Microbiome Dysbiosis-Mediated Neuroimmune Dysregulation and Protein Misfolding and Clearance in the Pathogenesis of Chronic Neurodegenerative Disorders.Frontiers in neuroscience · 2022Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain-intrinsic degenerative cascades have been proposed to be an initial factor driving lesion formation in multiple sclerosis (MS). Here, we identify neurodegeneration as a potent trigger for peripheral immune cell recruitment into the mouse forebrain. Female C57BL/6 mice were fed cuprizone for 3 weeks, followed by a period of 2 weeks on normal chow to induce the formation of lesion foci in the forebrain. Subsequent immunization with myelin oligodendrocyte glycoprotein 35-55 peptide, which induces myelin autoreactive T cells in the periphery, resulted in massive immune cell recruitment into the affected forebrain. Additional adoptive transfer experiments together with flow cytometry analysis underline the importance of brain-derived signals for immune cell recruitment. This study clearly illustrates the significance of brain-intrinsic degenerative cascades for immune cell recruitment and MS lesion formation. Additional studies have to address the signaling cascades and mechanistic processes that form the top-down communication between the affected brain area, neurovascular unit, and peripheral immune cells. SIGNIFICANCE STATEMENT: We identify neurodegeneration as a potent trigger for peripheral immune cell recruitment into the forebrain. Thus, immune cell recruitment might be a second step during the formation of new inflammatory lesions in multiple sclerosis. A better understanding of factors regulating neurodegeneration-induced immune cell recruitment will pave the way for the development of novel therapeutic treatment strategies.
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Registered trials
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