Demyelination induces selective vulnerability of inhibitory networks in multiple sclerosis
Zoupi, L.; Booker, S. A.; Eigel, D.; Werner, C.; Kind, P. C.; Spires-Jones, T.; Newland, B.; Williams, A.
Show abstract
In multiple sclerosis (MS), a chronic demyelinating disease of the central nervous system, neurodegeneration is detected early in the disease course and is associated with the long-term disability of patients. Neurodegeneration is linked to both inflammation and demyelination, but its exact cause remains unknown. This gap in knowledge contributes to the current lack of treatments for the neurodegenerative phase of MS. Here we ask if neurodegeneration in MS affects specific neuronal components and if it is the result of demyelination. Neuropathological examination of secondary progressive MS motor cortices revealed a selective vulnerability of inhibitory interneurons in MS. The generation of a rodent model of focal subpial cortical demyelination proved that this selective neurodegeneration is secondary to demyelination providing the first temporal evidence of demyelination-induced neurodegeneration and a new preclinical model for the study of neuroprotective treatments.
Matching journals
The top 6 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Microglia-neuron communication at nodes of Ranvier depends on neuronal activity through potassium release and contributes to myelin repair. 96%
- The transcriptional response of cortical neurons to concussion reveals divergent fates after injury 96%
- Pericyte-derived fibrotic scarring is conserved across diverse central nervous system lesions 96%
Similar papers in this journal
- Lymphotoxin-alpha expression in the meninges causes lymphoid tissue formation and neurodegeneration 94%
- Enhanced mGluR1 function causes motor deficits and region-specific Purkinje cell dysfunction 94%
- Cell-binding IgM in CSF is distinctive of multiple sclerosis and targets the iron transporter SCARA5 94%
Similar papers in this journal
- Meningeal inflammation in multiple sclerosis induces phenotypic changes in cortical microglia that differentially associate with neurodegeneration 96%
- Defects in lysosomal function and lipid metabolism in human microglia harboring a TREM2 loss of function mutation 94%
- From methylation to myelination: epigenomic and transcriptomic profiling of chronic inactive demyelinated multiple sclerosis lesions 94%
Similar papers in this journal
Similar papers in this journal
- Progressive axonopathy when oligodendrocytes lack the myelin protein CMTM5 96%
- MHC class I and MHC class II reporter mice enable analysis of immune oligodendroglia in mouse models of multiple sclerosis 95%
- Heterozygosity for neurodevelopmental disorder-associated TRIO variants yields distinct deficits in behavior, neuronal development, and synaptic transmission in mice. 95%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.