Published in Nature Neuroscience, the mouse study used MALDI imaging to map glucose across developing brain regions and link high glucose to dividing oligodendrocyte progenitor cells.
The team found ACLY drives glucose-linked histone acetylation needed for progenitor proliferation; deleting Acly caused temporary myelin loss, while a ketogenic diet improved deficits in mice.
Researchers said the developmental window mirrors roughly 32 to 40 weeks of human gestation, suggesting possible relevance for premature infants' white-matter injury and future myelin repair strategies, including multiple sclerosis.
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