Saturday, February 10, 2018

New Inroads Against Multiple Sclerosis

Read this.  Excerpts:

Medical progress against multiple sclerosis (MS) took a major leap forward in 2017 with the approval by the US Food and Drug Administration (FDA) of ocrelizumab, a drug that has shown success against 2 different forms of the disease. The year also brought further signs that it may be possible to biochemically reverse damage wrought by MS.

So, there’s a potentially effective monoclonal antibody drug, and there are possibilities of reversing the damage.  Stem cells are always useful for repair.

One of the key epidemiologic points about MS is that it has increased in frequency, and although there are now 203 genes that influence MS risk, all of these influences are very small effects, and the majority of susceptibility is not genetic and is almost certainly environmental. What in the environment is responsible for triggering MS is one of the great questions in MS research. It's unanswered but is likely to be a virus or bacterium. 
Dr Cohen:I would add that the microbe may not only be external to the person, but something in their own microbiome. It probably is not one single culprit, but many potential culprits. Or the distribution, the presence of some or absence of other microbial agents, may be what leads to susceptibility.

Once again, the microbiome.  Remember that your microbiome is influenced by diet.

Dr Hauser:It's likely that the microbiome has a substantial effect on MS in 2 ways. The first is the molecular mimicry, where some cell component of a bacterium or virus resembles a protein or substance in the brain. The second is that our microbiota influence the regulatory tone of our immune system, and that could lead to differences in the trajectory of disease after it begins. 
We don't yet know what the likely microbial culprit or culprits are. The strongest epidemiologic link to multiple sclerosis remains a late onset infection with the Epstein-Barr virus (EBV), [perhaps] the occurrence of infectious mononucleosis, but we really don’t know if EBV is causally linked or is a surrogate for some other infectious agent.

That’s also useful to know, and another avenue to explore for prevention of therapy, mostly the former.

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