Journal
ELIFE
Volume 5, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.18246
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Funding
- Third Military Medical University Overseas Youth Program Grant
- National Natural Science Foundation of China [NSCF31471043, 81270017]
- Deutsche Forschungsgemeinschaft Fellowship grants (DFG) [Le 3079/1-1]
- National Multiple Sclerosis Society [FG 2067-A-1, RG5203A4]
- Joint Research Fund [NSCF 31228011]
- Chongqing Scientific and Technical Innovation Foundation of China [CSTCKJCXLJRC07]
- Target ALS [A121679]
- National Institutes of Health [R01NS062796]
- Rachleff Endowment
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Demyelination in MS disrupts nerve signals and contributes to axon degeneration. While remyelination promises to restore lost function, it remains unclear whether remyelination will prevent axonal loss. Inflammatory demyelination is accompanied by significant neuronal loss in the experimental autoimmune encephalomyelitis (EAE) mouse model and evidence for remyelination in this model is complicated by ongoing inflammation, degeneration and possible remyelination. Demonstrating the functional significance of remyelination necessitates selectively altering the timing of remyelination relative to inflammation and degeneration. We demonstrate accelerated remyelination after EAE induction by direct lineage analysis and hypothesize that newly formed myelin remains stable at the height of inflammation due in part to the absence of MOG expression in immature myelin. Oligodendroglial-specific genetic ablation of the M1 muscarinic receptor, a potent negative regulator of oligodendrocyte differentiation and myelination, results in accelerated remyelination, preventing axonal loss and improving functional recovery. Together our findings demonstrate that accelerated remyelination supports axonal integrity and neuronal function after inflammatory demyelination.
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