Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Oligodendroglial Energy Metabolism and (re) Myelination

Version 1 : Received: 10 February 2021 / Approved: 11 February 2021 / Online: 11 February 2021 (10:57:28 CET)

How to cite: Tepavcevic, V. Oligodendroglial Energy Metabolism and (re) Myelination. Preprints 2021, 2021020277 (doi: 10.20944/preprints202102.0277.v1). Tepavcevic, V. Oligodendroglial Energy Metabolism and (re) Myelination. Preprints 2021, 2021020277 (doi: 10.20944/preprints202102.0277.v1).

Abstract

Central nervous system (CNS) myelin has a crucial role in accelerating the propagation of action potentials and providing trophic support to the axons. Defective myelination and lack of myelin regeneration following demyelination can both lead to axonal pathology and neurodegeneration. Energy deficit has been evoked as an important contributor to various CNS disorders, including multiple sclerosis (MS). This suggests that dysregulation of energy homeostasis in oligodendroglia may be an important contributor to myelin dysfunction and lack of repair observed in the disease. This article will focus on energy metabolism pathways in oligodendroglial cells and highlight differences dependent on the maturation stage of the cell. In addition, it will emphasize that the use of alternative energy sources by oligodendroglia may be required to save glucose for functions that cannot be fulfilled by other metabolites, thus ensuring sufficient energy input for both myelin synthesis and trophic support to the axons. Finally, it will point out that neuropathological findings in a subtype of MS lesions likely reflect defective oligodendroglial energy homeostasis in the disease.

Subject Areas

energy metabolism; oligodendrocyte; oligodendrocyte progenitor cell; myelin; remyelination; multiple sclerosis; glucose; ketone bodies; lactate; N-acetyl aspartate; demyelination

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