Interaction between Neurons and the Oligodendroglial Lineage in Multiple Sclerosis and Its Preclinical Models

Multiple sclerosis (MS) is a complex central nervous system inflammatory disease leading to demyelination and associated functional deficits. Though endogenous remyelination exists, it is only partial and, with time, patients can enter a progressive phase of the disease, with neurodegeneration as a hallmark. Though major therapeutic advances have been made, with immunotherapies reducing relapse rate during the inflammatory phase of MS, there is presently no therapy available which significantly impacts disease progression. Remyelination has been shown to favor neuroprotection, and it is thus of major importance to better understand remyelination mechanisms in order to promote them and hence preserve neurons. A crucial point is how this process is regulated through the neuronal crosstalk with the oligodendroglial lineage. In this review, we present the current knowledge on neuron interaction with the oligodendroglial lineage, in physiological context as well as in MS and its experimental models. We further discuss the therapeutic possibilities resulting from this research field, which might allow to support remyelination and neuroprotection and thus limit MS progression.

Automated summary

Multiple sclerosis is a complex inflammatory disease of the central nervous system characterized by neurodegeneration and demyelination. Understanding the mechanisms of remyelination is crucial for promoting neuroprotection and limiting disease progression. The interaction between neurons and the oligodendroglial lineage plays a significant role in potential therapeutic strategies for supporting remyelination and neuroprotection in MS.