Overview
- The Nature Neuroscience study, published Thursday, reports that local glucose levels in the developing brain tell progenitor cells when to multiply and when to mature into myelin-making cells.
- The team identifies ATP-citrate lyase as the key enzyme that generates nuclear acetyl-CoA for histone acetylation to drive cell division, and shows that deleting Acly in these cells reduces their numbers and causes temporary myelin loss in mice.
- Mice lacking ACLY in progenitors regained part of their myelin on a ketogenic diet, indicating that ketone bodies can bypass the glucose-dependent pathway to support myelin formation.
- Using MALDI imaging, researchers mapped region- and time-specific glucose gradients in mouse brains and tied high sugar to more cell division and lower sugar to earlier maturation.
- The developmental window aligns with roughly 32–40 weeks of human gestation, hinting at ways to protect preterm infants’ white matter and guide myelin repair research in diseases like multiple sclerosis, though clinical recommendations are premature.