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Brain glucose levels regulate OPC fate: high glucose → proliferation, low glucose → maturation. Acetyl-CoA from glucose drives histone acetylation for OPC division; ketone bodies substitute for myelin synthesis. Ketogenic diet rescues myelin in ACLY-deficient mice. Connects to: N-Dimensional Gene Hypothesis, PIST polymorphic shifter, topological state machine, FAMM delay lines, waveprobe manifolds |
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