Automated analysis of gray matter damage in aged mice reveals impaired remyelination in the cuprizone model.

Multiple sclerosis is a chronic autoimmune disease of the central nervous system characterized by myelin loss, axonal damage, and glial scar formation. Still, the underlying processes remain unclear, as numerous pathways and factors have been found to be involved in the development and progression of the disease. Therefore, it is of great importance to find suitable animal models as well as reliable methods for their precise and reproducible analysis.

Microglia-mediated demyelination protects against CD8 T cell-driven axon degeneration in mice carrying PLP defects.

Axon degeneration and functional decline in myelin diseases are often attributed to loss of myelin but their relation is not fully understood. Perturbed myelinating glia can instigate chronic neuroinflammation and contribute to demyelination and axonal damage. Here we study mice with distinct defects in the proteolipid protein 1 gene that develop axonal damage which is driven by cytotoxic T cells targeting myelinating oligodendrocytes.

Corrigendum: Polysialic acid promotes remyelination in cerebellar slice cultures by Siglec-E-dependent modulation of microglia polarization.

[This corrects the article DOI: 10.3389/fncel.2023.

Polysialic acid promotes remyelination in cerebellar slice cultures by Siglec-E-dependent modulation of microglia polarization.

Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system. Spontaneous restoration of myelin after demyelination occurs, but its efficiency declines during disease progression. Efficient myelin repair requires fine-tuning inflammatory responses by brain-resident microglia and infiltrating macrophages.

Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination.

Demyelination in the central nervous system (CNS) is a hallmark of many neurodegenerative diseases such as multiple sclerosis (MS) and others. Here, we studied astrocytes during de- and remyelination in the cuprizone mouse model. To this end, we exploited the ribosomal tagging (RiboTag) technology that is based on Cre-mediated cell type-selective HA-tagging of ribosomes.