Abstract
Failed regeneration of CNS myelin contributes to clinical decline in neuroinflammatory and neurodegenerative diseases, for which there is an unmet therapeutic need. Here we reveal that efficient remyelination requires death of proinflammatory microglia followed by repopulation to a pro-regenerative state. We propose that impaired microglia death and/or repopulation may underpin dysregulated microglia activation in neurological diseases, and we reveal therapeutic targets to promote white matter regeneration.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Corpus Callosum / drug effects
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Corpus Callosum / pathology
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Demyelinating Diseases / chemically induced
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Demyelinating Diseases / physiopathology*
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Female
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Gene Expression Profiling
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Humans
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Inflammation
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Lysophosphatidylcholines / toxicity
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Male
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Mice
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Mice, Inbred C57BL
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Microglia / classification
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Microglia / physiology*
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Multiple Sclerosis / pathology
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Necrosis
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Nerve Regeneration / physiology*
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Nestin / analysis
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Phagocytosis
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Rats
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Rats, Sprague-Dawley
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Sequence Analysis, RNA
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White Matter / physiology
Substances
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Lysophosphatidylcholines
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NES protein, human
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Nes protein, mouse
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Nestin