ArticleMolecular neurobiology2016
Lesion Expansion in Experimental Demyelination Animal Models and Multiple Sclerosis Lesions.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- CD44 as a Conserved Biomarker and Functional Modulator of Neuroinflammation in Multiple Sclerosis and Beyond.Molecular neurobiology · 2026Article
- N-butyl-β-carboline-3-carboxylate (β-CCB) systemic administration promotes remyelination in the cuprizone demyelinating model in mice.Scientific reports · 2024Article
- The Cuprizone Model: Dos and Do Nots.Cells · 2020Review
- Visualization of the Breakdown of the Axonal Transport Machinery: a Comparative Ultrastructural and Immunohistochemical Approach.Molecular neurobiology · 2019Article
- G-Protein-Coupled Receptor Gpr17 Expression in Two Multiple Sclerosis Remyelination Models.Molecular neurobiology · 2019Article
- Toll-Like Receptor 2-Mediated Glial Cell Activation in a Mouse Model of Cuprizone-Induced Demyelination.Molecular neurobiology · 2018Article
- Effect of Intrastriatal 6-OHDA Lesions on Extrastriatal Brain Structures in the Mouse.Molecular neurobiology · 2018Article
- Cuprizone-Containing Pellets Are Less Potent to Induce Consistent Demyelination in the Corpus Callosum of C57BL/6 Mice.Journal of molecular neuroscience : MN · 2017Article
- Intravenous transplantation of mouse embryonic stem cells attenuates demyelination in an ICR outbred mouse model of demyelinating diseases.Neural regeneration research · 2016Article
- Neurodegeneration Triggers Peripheral Immune Cell Recruitment into the Forebrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gray matter pathology is an important aspect of multiple sclerosis (MS) pathogenesis and disease progression. In a recent study, we were able to demonstrate that the higher myelin content in the white matter parts of the brain is an important variable in the neuroinflammatory response during demyelinating events. Whether higher white matter myelination contributes to lesion development and progression is not known. Here, we compared lesion size of intra-cortical vs. white matter MS lesions. Furthermore, dynamics of lesion development was compared in the cuprizone and lysophosphatidylcholine models. We provide clear evidence that in the human brain, white matter lesions are significantly increased in size as compared to intra-cortical gray matter lesions. In addition, studies using the cuprizone mouse model revealed that the autonomous progression of white matter lesions is more severe compared to that in the gray matter. Focal demyelination revealed that the application of equal amounts of lysophosphatidylcholine results in more severe demyelination in the white compared to the gray matter. In summary, lesion progression is most intense in myelin-rich white matter regions, irrespective of the initial lesion trigger mechanism. A better understanding of myelin debris-triggered lesion expansion will pave the way for the development of new protective strategies in the future.
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