NG2+ oligodendrocyte progenitor cells are among the most metabolically active cell populations in the aging brain. AMPK/mTOR dysregulation in OPCs may impair their differentiation capacity, contributing to white matter loss in neurodegeneration. This challenge asks whether restoring metabolic checkpoints (via AMPK activators or selective mTORC1 inhibitors) rescues OPC function. Falsifiable prediction: AMPK activation in aged OPCs should restore remyelination after cuprizone demyelination, measurable by MBP expression increase ≥40% versus vehicle controls.