Endogenous repair and development inspired therapy of neurodegeneration in progressive multiple sclerosis

ABSTRACT

Introduction: In recent years, there has been progress in understanding the etiology and immune mechanisms of multiple sclerosis (MS). however, for most, once the diagnosis is made, significant pathology is already present in the central nervous system (CNS), and in many, this leads to neurodegeneration, which accumulates in disability. although, the mechanisms of such progression are poorly understood, new data suggest lack of remyelination paired with dysfunction of neurons along with stem and progenitor cells as the basis and recent developmental studies suggest that cns repair processes share mechanisms with development.

Areas covered: Here, the authors examine the neurodevelopmental processes that may be reactivated to gain a better understanding of regeneration under pathological conditions. Specifically, the authors focus on the molecular framework of these mechanisms, signaling pathways in neuron and oligodendrocyte development, and provide evidence that the activation of these processes can help us design new therapeutic avenues to halt progression.

Expert commentary: Accumulating evidence indicates that there is no single mechanism of progression in MS; instead there is heterogeneity in which repair processes are perturbed. Together, this not only poses a challenge for treatment, but also at the benchside, when prioritizing which developmental targets warrant investigation in future trials.

KEYWORDS:

• Neural stem cells
• immunity
• axonal regeneration
• genomics
• migration

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Additional information

Funding

This paper was not funded.