Research: Nerve signalling targetted in early onset MS

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AS Dhaunchak AS et al. Implication of perturbed axoglial apparatus in early pediatric multiple sclerosis. Annals Neurol. DOI: 10.1002/ana.22693 [Epub ahead of Print]

Cerebrospinal fluid samples collected from children during initial presentation of CNS-inflammation, that may or may not subsequently be diagnosed as multiple sclerosis (MS), were subjected to large-scale proteomics screen. Unexpectedly, major compact myelin membrane proteins typically implicated in MS were not detected. However, multiple molecules that localize to the node of Ranvier and the surrounding axoglial apparatus membrane were implicated, indicating perturbed axon-glial interactions in those children destined for diagnosis of MS.

If we look at the cerebrospinal fluid from children with neurological symptoms and then look at whether they go on to develop MS or not, thoses that developed MS, showed evidence of damage to the nodes of ranvier, rather than oligodendrocyte and myelin proteins. Therefore, are the early targets in MS, nerve conduction proteins rather than myelin. Yet further dints in the autoimmune hypothesis perhaps.

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MouseDoctor

6 comments

  • From an engineering point of view, this is the weakest part of the axon continuum. The same goes for the oligodendrocyte "legs" that reach and myelinate the axons. So, both areas are more susceptible to an internal sudden impact.

    It's known that macrophages clear up myelin debris in complete absence of other immune cells (Prineas). This study provides support to the idea that these debris are formed after an injurious impact on the oligodendrocyte support system.

  • Sudden impact, what is the impact?

    Am I really asking this? Do I want the answer?

    Hope it has nothing to do with blood flow.

  • I would prefer a comment on the idea that nodes of Ranvier could be early damaged because of their smaller diameter. If that was true, then a mechanical explanation would be inevitable, however unexpected.

  • I'm not quite sure why this dents the autoimmune hypothesis. The nodes of Ranvier are being perturbed by something. Surely it may just be that their proteins are reacting first to attack before myelin proteins, but we just haven't been able to see it earlier?

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