Figure 8: Working model of repair processes influenced by cholesterol.
From: Dietary cholesterol promotes repair of demyelinated lesions in the adult brain
Working model of nutritional cholesterol mediated repair processes. Cuprizone exposure causes oligodendrocyte loss and demyelination and slow repair (left panel) because of OPC depletion, imbalanced growth factors, and low local availability of cholesterol. In case of nutritional supplementation, cholesterol from the circulation enters the CNS because of increased BBB permeability (red arrows) increasing the local cholesterol availability (1). There, cholesterol rebalances the expression of growth factors and mitogens synthesized e.g. by astrocytes (2). This simultaneously enhances OPC proliferation (3) and opens a window for OPC differentiation. Cholesterol directly facilitates oligodendrocyte differentiation, presumably by relieving cells from time and energy intensive cholesterol synthesis (4). Altogether, these effects provide a ‘fast track’ to remyelination and repair (5).
