Highlights d Injury-induced mitochondrial dysfunction contributes to CNS axonal regenerative failure d Enhancing its transport recovers mitochondrial integrity after spinal cord injury (SCI) d Removing a mitochondrial anchor protein enhances functional recovery after SCI d Increasing energy metabolism via creatine treatment promotes axon regeneration after SCI
The unique polarization and high‐energy demand of neurons necessitates specialized mechanisms to maintain energy homeostasis throughout the cell, particularly in the distal axon. Mitochondria play a key role in meeting axonal energy demand by generating adenosine triphosphate through oxidative phosphorylation. Recent evidence demonstrates how axonal mitochondrial trafficking and anchoring are coordinated to sense and respond to altered energy requirements. If and when these mechanisms are impacted in pathological conditions, such as injury and neurodegenerative disease, is an emerging research frontier. Recent evidence also suggests that axonal energy demand may be supplemented by local glial cells, including astrocytes and oligodendrocytes. In this review, we provide an updated discussion of how oxidative phosphorylation, aerobic glycolysis, and oligodendrocyte‐derived metabolic support contribute to the maintenance of axonal energy homeostasis.
See Pluchino and Peruzzotti-Jametti (doi:) for a scientific commentary on this article.Macrophages have a critical role in remyelination. Psachoulia et al. show that IL4I1, a macrophage-secreted enzyme, promotes CNS remyelination by modulating T cell driven inflammation after focal demyelination in mice. Injection of recombinant IL4I1 protein reverses disease progression in a mouse model of multiple sclerosis, resulting in recovery from hindlimb paralysis.
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