Effect of nitric oxide to axonal degeneration in multiple sclerosis via downregulating monocarboxylate transporter 1 in oligodendrocytes

- Analyzed the mechanism how NO induces mitochondrial dysfunction in neurons and glial cells from a balanced view.
- Described the role of MCT1 in energy mechanism of MS, and decrease of MCT1 may account for axonal energy deficit.
- Hypothesized that NO-induced MCT1 downregulation in OLs may involve in axonal degeneration, and eventually leads to MS.

Multiple sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS). Axonal degeneration, one of the main pathological characteristics of MS, is affected by nitric oxide (NO). In turn, NO induces mitochondrial dysfunction of neurons and glial cells. Inadequate glucose causes monocarboxylate transporter 1 (MCT1) to transfer lactate from oligodendrocytes (OLs) to neurons, which decreases MCT1 and results in energy substrate deficit (mainly lactate) in axons. The condition gradually leads to axonal degeneration. This study proposes that NO-induced MCT1 down-regulation in OLs may be involved in the pathological process of axonal degeneration, which eventually leads to MS.