Inducing neuronal mitochondrial activity during central nervous system inflammation counteracts inflammation-induced neuronal electron transport chain deficiency and calcium toxicity, thereby protecting against neuronal loss in a multiple sclerosis mouse model.

Imaging mass cytometry simultaneously lights up distinct immune cells in the brain.

Computational-driven, imaging-based topological profiles of neurodegeneration differ substantially in different neurodegenerative conditions, suggesting distinct modes of dependence of the pathological spread on the underlying connectivity.

Pain sensation induces relapse in a mouse model of multiple sclerosis via a sensory-sympathetic signaling pathway.

Oligodendrocytes with an enhanced ability to withstand cytotoxic stress display an increased capacity to remyelinate demyelination lesions of the CNS in the presence of an inflammatory environment.

Antigen-specific control of CD4+ T cell trans-migration by brain endothelial cells via presentation of CNS-derived antigens in MHC-II molecules.

Regeneration of oligodendrocytes in the cerebral cortex results in reorganization of the pattern of myelination, potentially impacting information processing within cortical networks in diseases such as multiple sclerosis.

A novel EAE model featuring cortical lesions and an autoimmune heterogeneity, two key parameters missing in the classical model, allows for insights in disease pathogenesis.

A link between chronic stress and organ dysfunction is explained by the gateway reflex, in which brain micro-inflammation at specific vessels establishes a new neural pathway to induce fatal organ failure particularly in gastrointestine and heart.

Heparan sulfate synthesis by mature oligodendrocytes creates a protective and permissive environment controling microglia and oligodendrocyte progenitors reactivation during remyelination.