ArticleMolecular neurobiology2019
Impaired Remyelination in a Mouse Model of Huntington Disease.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- The role of oligodendroglial dysfunction in Huntington's disease.Journal of Huntington's disease · 2025Review
- The Effect of Probiotics and Microbiota on Nervous System and Mental Illnesses.Central nervous system agents in medicinal chemistry · 2025Review
- Environmental Deprivation Effects on Myelin Ultrastructure in Huntington Disease and Wildtype Mice.Molecular neurobiology · 2024Article
- Early whole-body mutant huntingtin lowering averts changes in proteins and lipids important for synapse function and white matter maintenance in the LacQ140 mouse model.Neurobiology of disease · 2023Article
- Early whole-body mutant huntingtin lowering averts changes in proteins and lipids important for synapse function and white matter maintenance in the LacQ140 mouse model.bioRxiv : the preprint server for biology · 2023Article
- Pain in Huntington's disease and its potential mechanisms.Frontiers in aging neuroscience · 2023Review
- Huntington disease oligodendrocyte maturation deficits revealed by single-nucleus RNAseq are rescued by thiamine-biotin supplementation.Nature communications · 2022Article
- Early white matter pathology in the fornix of the limbic system in Huntington disease.Acta neuropathologica · 2021Article
- Utilising Induced Pluripotent Stem Cells in Neurodegenerative Disease Research: Focus on Glia.International journal of molecular sciences · 2021Review
- Gut-Brain Axis: Role of Gut Microbiota on Neurological Disorders and How Probiotics/Prebiotics Beneficially Modulate Microbial and Immune Pathways to Improve Brain Functions.International journal of molecular sciences · 2020Review
- Erucic acid, a nutritional PPARδ-ligand may influence Huntington's disease pathogenesis.Metabolic brain disease · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
White matter (WM) abnormalities are a well-established feature of Huntington disease (HD), although their nature is not fully understood. Here, we asked whether remyelination as a measure of WM plasticity is impaired in a model of HD. Using the cuprizone assay, we examined demyelination and remyelination responses in YAC128 HD mice. Treatment with 0.2% cuprizone (CPZ) for 6 weeks resulted in significant reduction in mature (GSTπ-positive) oligodendrocyte counts and FluoroMyelin staining in the corpus callosum, leading to similar demyelination states in YAC128 and wild-type (WT) mice. Six weeks following cessation of CPZ, we observed robust remyelination in WT mice as indicated by an increase in mature oligodendrocyte counts and FluoroMyelin staining. In contrast, YAC128 mice exhibited an impaired remyelination response. The increase in mature oligodendrocyte counts in YAC128 HD mice following CPZ cessation was lower than that of WT. Furthermore, there was no increase in FluoroMyelin staining compared to the demyelinated state in YAC128 mice. We confirmed these findings using electron microscopy where the CPZ-induced reduction in myelinated axons was reversed following CPZ cessation in WT but not YAC128 mice. Our findings demonstrate that remyelination is impaired in YAC128 mice and suggest that WM plasticity may be compromised in HD.
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Registered trials
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