Klaus-Armin Nave, Max Planck Institute of Experimental Medicine, Göttingen, Germany : « Novel roles of oligodendrocytes in axonal energy metabolism ».
Friday, February 15, 2013 at 11:30 am
Oligodendrocytes make myelin to speed up axonal impulse propagation and to reduce overall energy consumption in the brain. This function is illustrated by severe neurological defects and premature death in mouse and man with developmental defects of myelination (leukodystrophy). Importantly, the electrically insulating myelin sheath may also deprive axons from free access to extracellular metabolites, posing an inherent “risk of myelination” that is obviously overcome by intact oligodendrocytes. This view is supported by the phenotype of mice with mutations in the oligodendrocyte-specific genes Plp1 and Cnp1, which had revealed that intact oligodendrocytes are required to preserve long-term axonal integrity. The supportive function of oligodendrocytes is independent of myelin itself and may be regulated by SIRT2, an NAD+-dependent protein deacetylase. We have hypothesized that long axons require associated glial cells to meet their metabolic demands. We can now provide direct evidence that oligodendrocytes provide glycolysis products that support mitochondrial energy metabolism in long axonal tracts. Such metabolic support of axon function is not only relevant for human myelin diseases, but also other neurological disorders as long axons are the bottle neck of neuronal integrity.
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